PSA Cancer Research Results
PSA, prostate-specific antigen: Click to Expand ⟱
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Prostate-Specific Antigen (PSA) is a protein produced by both normal and malignant cells of the prostate gland. PSA testing is commonly used as a screening tool for prostate cancer.
Elevated levels of PSA in the blood can indicate the presence of prostate cancer, but they can also be caused by other conditions, such as benign prostatic hyperplasia (BPH) or prostatitis (inflammation of the prostate).
PSA is a clinical biomarker.
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Scientific Papers found: Click to Expand⟱
PSA↓, one patient
OS↑,
PSA↓,
cycD1/CCND1↓, cyclinD1 and cyclinD2
cycE/CCNE↓,
CDK2↓,
CDK4/6↓,
P21↑,
AR↓,
chemoPv↑, considerable potential for apigenin to be developed as a cancer chemopreventive agent.
ITGB4↓, apigenin inhibits hepatocyte growth factor-induced MDA-MB-231 cells invasiveness and metastasis by blocking Akt, ERK, and JNK phosphorylation and also inhibits clustering of β-4-integrin function at actin rich adhesive site
TumCI↓,
TumMeta↓,
Akt↓,
ERK↓,
p‑JNK↓,
*Inflam↓, The anti-inflammatory properties of apigenin are evident in studies that have shown suppression of LPS-induced cyclooxygenase-2 and nitric oxide synthase-2 activity and expression in mouse macrophages
*PKCδ↓, Apigenin has been reported to inhibit protein kinase C activity, mitogen activated protein kinase (MAPK), transformation of C3HI mouse embryonic fibroblasts and the downstream oncogenes in v-Ha-ras-transformed NIH3T3 cells (43, 44).
*MAPK↓,
EGFR↓, Apigenin treatment has been shown to decrease the levels of phosphorylated EGFR tyrosine kinase and of other MAPK and their nuclear substrate c-myc, which causes apoptosis in anaplastic thyroid cancer cells
CK2↓, apigenin has been shown to inhibit the expression of casein kinase (CK)-2 in both human prostate and breast cancer cells
TumCCA↑, apigenin induces a reversible G2/M and G0/G1 arrest by inhibiting p34 (cdc2) kinase activity, accompanied by increased p53 protein stability
CDK1↓, inhibiting p34 (cdc2) kinase activity
P53↓,
P21↑, Apigenin has also been shown to induce WAF1/p21 levels resulting in cell cycle arrest and apoptosis in androgen-responsive human prostate cancer
Bax:Bcl2↑, Apigenin treatment has been shown to alter the Bax/Bcl-2 ratio in favor of apoptosis, associated with release of cytochrome c and induction of Apaf-1, which leads to caspase activation and PARP-cleavage
Cyt‑c↑,
APAF1↑,
Casp↑,
cl‑PARP↑,
VEGF↓, xposure of endothelial cells to apigenin results in suppression of the expression of VEGF, an important factor in angiogenesis via degradation of HIF-1α protein
Hif1a↓,
IGF-1↓, oral administration of apigenin suppresses the levels of IGF-I in prostate tumor xenografts and increases levels of IGFBP-3, a binding protein that sequesters IGF-I in vascular circulation
IGFBP3↑,
E-cadherin↑, apigenin exposure to human prostate carcinoma DU145 cells caused increase in protein levels of E-cadherin and inhibited nuclear translocation of β-catenin and its retention to the cytoplasm
β-catenin/ZEB1↓,
HSPs↓, targets of apigenin include heat shock proteins (61), telomerase (68), fatty acid synthase (69), matrix metalloproteinases (70), and aryl hydrocarbon receptor activity (71) HER2/neu (72), casein kinase 2 alpha
Telomerase↓,
FASN↓,
MMPs↓,
HER2/EBBR2↓,
CK2↓,
eff↑, The combination of sulforaphane and apigenin resulted in a synergistic induction of UGT1A1
AntiAg↑, Apigenin inhibit platelet function through several mechanisms including blockade of TxA
eff↑, ex vivo anti-platelet effect of aspirin in the presence of apigenin, which encourages the idea of the combined use of aspirin and apigenin in patients in which aspirin fails to properly suppress the TxA
FAK↓, Apigenin inhibits expression of focal adhesion kinase (FAK), migration and invasion of human ovarian cancer A2780 cells.
ROS↑, Apigenin generates reactive oxygen species, causes loss of mitochondrial Bcl-2 expression, increases mitochondrial permeability, causes cytochrome C release, and induces cleavage of caspase 3, 7, 8, and 9 and the concomitant cleavage of the inhibitor
Bcl-2↓,
Cyt‑c↑,
cl‑Casp3↑,
cl‑Casp7↑,
cl‑Casp8↑,
cl‑Casp9↑,
cl‑IAP2/BIRC3↑,
AR↓, significant decrease in AR protein expression along with a decrease in intracellular and secreted forms of PSA. Apigenin treatment of LNCaP cells
PSA↓,
p‑pRB↓, apigenin inhibited hyperphosphorylation of the pRb protein
p‑GSK‐3β↓, Inhibition of p-Akt by apigenin resulted in decreased phosphorylation of GSK-3beta.
CDK4↓, both flavonoids exhibited cell growth inhibitory effects which were due to cell cycle arrest and downregulation of the expression of CDK4
ChemoSen↑, Combination therapy of gemcitabine and apigenin enhanced anti-tumor efficacy in pancreatic cancer cells (MiaPaca-2, AsPC-1)
Ca+2↑, apigenin in neuroblastoma SH-SY5Y cells resulted in increased apoptosis, which was associated with increases in intracellular free [Ca(2+)] and Bax:Bcl-2 ratio, mitochondrial release of cytochrome c and activation of caspase-9, calpain, caspase-3,12
cal2↑,
*antiOx↑, ASX has protective effects on various diseases, such as Parkinson’s disease and cancer by showing potent antioxidant and anti-inflammatory properties.
*Inflam↓,
ChemoSen↑, Additionally, we determined that it exhibited synergistic action with cisplatin and significantly enhanced apoptotic cell death in PCa cells. (beware of dose required for this?)
E-cadherin↑, graphical abstract
N-cadherin↓,
VEGF↓,
cMyc↓,
PSA↓,
cl‑Casp3↑, ASTX improves the cisplatin induces caspase 3 cleavage and PARP1 activation
PARP1↑,
Dose↝, Bicalutamide is a nonsteroidal pure antiandrogen given at a dosage of 150 mg once daily as monotherapy for the treatment of early (localised or locally advanced) nonmetastatic prostate cancer.
BioAv↑, Bicalutamide is slowly and saturably absorbed, but absorption is unaffected by food.
Half-Life↑, It has a long plasma elimination half-life (1 week) and accumulates about 10-fold in plasma during daily administration.
CYP3A4↓, In vitro data suggest that (R)-bicalutamide has the potential to inhibit CYP3A4 and, to a lesser extent, CYP2C9, 2C19 and 2D6.
PSA↓, Bicalutamide produces a dose-related decrease in prostate-specific antigen (PSA) at dosages < or = 150 mg/day.
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Review, |
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NA |
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Review, |
AD, |
NA |
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Risk↓, Boron reduces prostate cancer incidence by up to 64%
serineP↓, Boric acid acts to inhibit serine proteases—it decreases PSA by 87% and reduces tumor size in a prostate cancer mouse model
PSA↓,
TumVol↓,
IGF-1↓, expression of IGF-1 (insulin-like growth factor type 1) was markedly reduced by boron treatment. Circulating blood levels of IGF-1 were not reduced in the treated mice, however.
*Mag↑, In situations of adequate calcium supply but deficient magnesium resources, boron appears to substitute or “pinch hit” for magnesium during the process of bone formation.
*Calcium↑, The effect of boron on raising plasma calcium levels may, in part, be due to its enhancing effect on vitamin D.1
*VitD↑,
*COX2/PTGS2↓, boron has been shown to inhibit cyclooxygenase (COX) and lipoxygenase (LOX).
*5LO↓,
*PGE2↓, leads to a decrease in prostaglandin E2 (PGE2)
*NF-kB↓, suppressing nuclear factor kappa beta (NfkappaB)
*cognitive↑, Since it is now commonly accepted that the routine use of NSAIDs significantly reduces the incidence of Alzheimer’s disease,31,32 it is not surprising that papers have been published on boron’s positive effect on cognitive function.
*hs-CRP↓, reduces levels of inflammatory biomarkers, such as high-sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor μ (TNF-μ);
*TNF-α↓,
*SOD↑, raises levels of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase
*Catalase↑,
*GPx↑,
*cognitive↑, improves the brains electrical activity, cognitive performance, and short-term memory for elders; restricted boron intake adversely affected brain function and cognitive performance.
*memory↑, In humans, boron deprivation (<0.3 mg/d) resulted in poorer performance on tasks of motor speed and dexterity, attention, and short-term memory.
*Risk↓, Boron-rich diets and regions where the soil and water are rich in boron correlate with lower risks of several types of cancer, including prostate, breast, cervical, and lung cancers.
*SAM-e↑,
*NAD↝, Boron strongly binds oxidized NAD+,76 and, thus, might influence reactions in which NAD+ is involved
*ATP↝,
*Ca+2↝, Because of its positive charge, magnesium stabilizes cell membranes, balances the actions of calcium, and functions as a signal transducer
HDAC↓, some boronated compounds are histone deacetylase inhibitors
TumVol↓,
IGF-1↓, expression of IGF-1 in the tumors was significantly reduced by boron treatment
PSA↓, Boronic acid has been shown to inhibit PSA activity.
Cyc↓, boric acid inhibits the growth of prostate-cancer cells both by decreasing expression of A-E cyclin
TumCMig↓,
*serineP↓, Boron exists in the human body mostly in the form of boric acid, a serine protease inhibitor.
HIF-1↓, shown to greatly inhibit hypoxia-inducible factor (HIF) 1
*ChemoSideEff↓, An in vitro study found that boric acid can help protect against genotoxicity and cytotoxicity that are induced in lymphocytes by paclitaxel
*VitD↑, greater production of 25-hydroxylase, and, thus, greater potential for vitamin-D activation
*Mag↑, Boron significantly improves magnesium absorption and deposition in bone
*eff↑, boron increases the biological half-life and bioavailability of E2 and vitamin D.
Risk↓, risk of prostate cancer was 52% lower in men whose diets supplied more than 1.8 mg/d of boron compared with those whose dietary boron intake was less than or equal to 0.9 mg/d.
*Inflam↓, As research into the chemistry of boron-containing compounds has increased, they have been shown to be potent antiosteoporotic, anti-inflammatory, and antineoplastic agents
*neuroP↑, In addition, boron has anti-inflammatory effects that can help alleviate arthritis and improve brain function and has demonstrated such significant anticancer
*Calcium↑, increase serum levels of estradiol and calcium absorption in peri- and postmenopausal women.
*BMD↑, boron stimulates bone growth in vitamin-D deficient animals and alleviates dysfunctions in mineral metabolism characteristic of vitamin-D deficiency
*chemoP↑, may help ameliorate the adverse effects of traditional chemotherapeutic agents. boric acid can help protect against genotoxicity and cytotoxicity that are induced in lymphocytes by paclitaxel, an anticancer drug commonly used to treat breast, ovarian
AntiCan↑, demonstrated preventive and therapeutic effects in a number of cancers, such as prostate, cervical, and lung cancers, and multiple and non-Hodgkin’s lymphoma
*Dose↑, only an upper intake level (UL) of 20 mg/d for individuals aged ≥ 18 y.
*Dose↝, substantial number of articles showing benefits support the consideration of boron supplementation of 3 mg/d for any individual who is consuming a diet lacking in fruits and vegetables
*BMPs↑, Boron was also found to increase mRNA expression of alkaline phosphatase and bone morphogenetic proteins (BMPs)
*testos↑, 1 week of boron supplementation of 6 mg/d, a further study by Naghii et al20 of healthy males (n = 8) found (1) a significant increase in free testosterone,
angioG↓, Inhibition of tumor-induced angiogenesis prevents growth of many types of solid tumors and provides a novel approach for cancer treatment; thus, HIF-1 is a target of antineoplastic therapy.
Apoptosis↑, Cancer cells, however, commonly overexpress sugar transporters and/or underexpress borate export, rendering sugar-borate esters as promising chemopreventive agents
*selectivity↑, In normal cells, the 2 latter, cell-destructive effects do not occur because the amount of borate present in a healthy diet, 1 to 10 mg/d, is easily exported from normal cells.
*chemoPv↑, promising chemopreventive agents
PSA↓, PSA activity is inhibited in vitro by boric acid
eff↑, newly developed boron-containing compounds have already demonstrated highly promising activities
*toxicity↓, Boronic acid/ester has been successfully incorporated into cancer treatments and therapy mainly due to its remarkable oxophilicity and low toxicity levels in the body
ROS↑, can trigger tumour microenvironmental abnormalities such as high levels of reactive oxygen species (ROS) and overexpressed enzymes
LAT↓, boron accumulation were observed to counterpart LAT-1 expression in a bone metastasis model of breast cancer
AntiCan↑, high concentration of boron in males reduces the probability of prostate cancer by 54% compared to males with low boron concentrations
AR↓, bortezomib
PSMB5↓, bortezomib
IGF-1↓, insulin-like growth factor 1 (IGF-1) in tumours was markedly reduced by boric acid.
PSA↓, exposure to both low-and high-dose boron supplementation, prostate-specific antigen (PSA) levels dropped by an average of 87%, while tumour size declined by an average of 31.5%
TumVol↓,
eff↑, phenylboronic acid is a more potent inhibitor than boric acid in targeting metastatic and proliferative properties of prostate cancer cells
Rho↓, RhoA, Rac1
Cdc42↓,
Ca+2↓, ER Ca+2 depletion occurred after the treatment of DU-145 prostate cancer cells with the physiological concentrations of boric acid
eff↑, boric acid (BA), sodium pentaborate pentahydrate (NaB), and sodium perborate tetrahydrate (SPT) against SCLC cell line using DMS-114 cells
TumVol↓, 38%
IGF-1↓, in tumors
PSA↓, 89%
PSA↓,
NAD↝, high affinity for the ribose moieties of NAD+
SAM-e↝, high affinity for S-adenosylmethione
PSA↓,
IGF-1↓,
Cyc↓, reduction in cyclins A–E
P21↓,
p‑MEK↓,
p‑ERK↓, ERK (P-ERK1/2)
ROS↑, induce oxidative stress by decreasing superoxide dismutase (SOD) and catalase (CAT)
SOD↓,
Catalase↓,
MDA↑,
GSH↓,
IL1↓, IL-1α
IL6↓,
TNF-α↓,
BRAF↝,
MAPK↝,
PTEN↝,
PI3K/Akt↝,
eIF2α↑,
ATF4↑,
ATF6↑,
NRF2↑,
BAX↑,
BID↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Bcl-xL↓,
*Half-Life↝, (Boron) is excreted with a half-life of 21 hours, and is mostly eliminated with only a low level of accumulation in bone.
*eff↑, 13 subjects predetermined to be vitamin D deficient found that during a 60-day supplementation period with 6 mg boron/day, serum 25-hydroxyvitamin D levels rose by an average of 20%
PSA↓, one study using nude mice implanted with human prostate adenocarcinoma (LNCaP) cells found that boron supplementation reduced serum prostate-specific antigen (PSA) levels, and reduced tumor size and expression of IGF-1,
TumVol↓,
IGF-1↓,
*memory↓, Boron deprivation : results in significantly poorer performance on tasks involving eye-hand coordination, attention, and short-term memory (Penland 1994 and 1998).
*motorD↓,
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Pca, |
LNCaP |
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Pca, |
PC3 |
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PC, |
DU145 |
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AR↓, Phytonutrients synergistically inhibit androgen signaling
ARE/EpRE↑, x4 the sum of single ingredients
TumCP↓, Phytonutrients inhibit prostate cancer cell proliferation
PSA↓, combination
of three compounds such as in the case of curcumin, vitamin E
and the tomato extract showed a stronger synergistic effect than
each pair of compounds. The inhibition of PSA secretion
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Pca, |
PC3 |
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Pca, |
LNCaP |
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in-vitro, |
Pca, |
DU145 |
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in-vivo, |
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NA |
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TumCP↓, profound antiproliferative effect on prostate cancer cells, inducing the apoptosis of both androgen receptor (AR)-positive (LNCaP) and -negative (PC-3, DU-145) prostate cancer cell lines
P53↑, increase of p53, p21, and Bax
P21↑,
BAX↑,
PSA↓, Capsaicin down-regulated the expression of not only prostate-specific antigen (PSA) but also AR
AR↓,
NF-kB↓, Capsaicin inhibited NF-kappa activation by preventing its nuclear migration
Proteasome↓, capsaicin inhibits proteasome activity which suppressed the degradation of IkappaBalpha
TumVol↓, Capsaicin, when given orally, significantly slowed the growth of PC-3 prostate cancer xenografts
eff∅, However, our experiments using the three TRVP1-inhibitors capsazepine, ruthenium red, and SB366791, did not show any attenuation of the inhibitory activity of capsaicin.
PSA↓, A decrease in serum prostate specific antigen (PSA) was observed on the PolyE arm
other↑, A significant increase in plasma EGCG concentration was achieved in the treatment arm at 6 and 12 months
Risk↝, was well tolerated but did not reduce the likelihood of a subsequent PCa diagnosis in men with baseline HGPIN or ASAP.
AR↓, Curcumin significantly decreased AR expression at both the mRNA and protein level.
PSA↓, PSA levels tended to be reduced in the curcumin group
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AR↓, results indicate that one of the potential mechanisms for the anticancer effect of the curcumin analogues was inhibition of AR pathways in human prostate cancer cells.
PSA↓, F10 and E10 resulted in a marked decrease in the level of PSA while the other compounds (curcumin, A10, B10 and C10) were less active.
Dose↑, However, in these studies, curcumin was used at relatively high concentrations, typically at >20 μM. I
PSA↓,
TGF-β↓, down regulation of the expression of TGF-β and an up-regulation of the bone morphogenic protein BMP-2 as a result of curcumin feeding
BMPs↑, BMP2,7
TumMeta↓, Curcumin Inhibits Prostate Cancer Bone Metastasis
PSA↓, The proportion of patients with PSA progression during the active curcumin treatment period (6 months) was significantly lower in the curcumin group than the placebo group (
Dose↝, two capsules, three times a day (1440 mg/day), for 6 months from the
beginning of ADT withdrawal.
PSA↓, Curcumin presumably synergizes with isoflavones to suppress PSA production in
prostate cells through the anti-androgen effects.
AR↓,
*toxicity↓, A reduction in systemic toxicity, statistically significant for neutropenia, associated with better results in term of OR rate, ICR, and BR were observed in group B compared with group A.
chemoP↑, ellagic acid as support therapy reduces chemotherapy induced toxicity, in particular neutropenia, in HRCP patients
Neut↑,
PSA↓, In group B, serum PSA concentrations markedly declined (>75%)
Dose↝, After reviewing the literature, a daily dose of 180 mg (60 g/every 8 h) active principle was selected and administered orally before meals with water (200–250 ml) throughout the chemotherapy cycles and during the period between cycles.
TumCG↓, EGCG, inhibited LNCaP cell growth and the expression of androgen regulated PSA and hK2 genes.
PSA↓,
HK2↓,
AR↓, decrease in androgen receptor protein with treatments of the tea polyphenols EGCG, GCG and theaflavins.
Sp1/3/4↓, Sp1 is the target for the tea polyphenols because treatments of EGCG decreased the expression, DNA binding activity and transactivation activity of Sp1 protein.
*chemoPv↑, Fisetin has been reported as a chemopreventive/chemotherapeutic agent in several types of cancer and also as a neuroprotective agent.
*neuroP↑,
*antiOx↑, Several studies indicate that fisetin is a promising novel antioxidant. The trolox-equivalent activity concentration (TEAC) value of fisetin has been reported to be 2.80±0.06 (
*GSH↑, Fisetin has been shown to increase intracellular glutathione (GSH) levels in the mouse hippocampal HT-22 cells both in the presence and absence of glutamate
*HO-1↑, the effect of fisetin on the upregulation of heme oxygenase-1 (HO-1)
*NRF2↑, Treatment with fisetin caused increased Nrf2 nuclear translocation and activity.
angioG↓, fisetin may reduce angiogenesis and consequently suppress tumor growth through inhibition of urokinase plasminogen activator (uPA)
TumCG↓,
uPA↓,
MMP1↓, fisetin to be a potent inhibitor of the matrix metalloproteinase (MMP)-1 activity
tumCV↓, Lung Decreased cancer cell viability and clonogenecity, increased PTEN, decreased PI3-K and Akt phosphorylation, activated TSC and AMPK, decreased phosphorylation and activation of mTOR,
PTEN↑,
PI3K↓, Fisetin also acts as a dual inhibitor of PI3K/Akt and mTOR signaling in prostate cancer cells
p‑Akt↓,
AMPK↑,
mTOR↓,
EGFR↓, Inhibited EGFR and NF-κB, decreased COX2 and PGE2, inhibited Wnt/β-catenin signaling, downregulated TCF-4, decreased cyclin D1 and MMP-7
NF-kB↓,
COX2/PTGS2↓,
PGE2↓,
Wnt↓,
β-catenin/ZEB1↓,
TCF↓,
cycD1/CCND1↓,
MMP7↓,
RadioS↑, Enhanced radiosensitivity of p53-mutant colon cancer cells, augmented radiation-induced G2/M arrest and apoptosis
PSA↓, Prostate Slowed tumor growth, decreased serum PSA levels
Securin↓, Moreover, fisetin inhibited securin expression regardless of p53 status,
TumCCA↑, accompanied by arrest of cells in the G0/G1 phase of the cell cycle
XIAP↓, fisetin treatment resulted in a decrease in the activity of NF-κB/p65, MMP-9, and X-linked inhibitor of apoptosis (XIAP)
*ERK↑, fisetin was the most effective flavonoid that induced neurite outgrowth by inducing ERK1/2 activation
*p‑CREB↑, Fisetin activated ERK1/2 and induced cAMP-response element-binding protein (CREB) phosphorylation in rat hippocampal slices and enhanced object recognition in mice.
*memory↑,
*GSH↑, It acts as an antioxidant, increases GSH, maintains mitochondrial function in the presence of oxidative stress, has anti-inflammatory activity against microglial cells, and inhibits the activity of 5-lipoxygenase,
*Inflam↓,
*5LO↓,
*memory↑, Oral administration of fisetin was shown to enhance learning and memory in mice [10]. In addition, it has anti-inflammatory activity and has been shown to inhibit the activity of 5-lipoxygenase in microglia cells,
*Inflam↓,
*5LO↓,
*lipid-P↓, thereby reducing the production of lipid peroxides and their pro-inflammatory by-products
*NF-kB↓, Of the nine different flavones tested, fisetin was the most potent in suppressing tumor necrosis factor (TNF)-induced NF-κB activation.
*antiOx↑, Fisetin not only has direct antioxidant activity but can also increase the intracellular levels of glutathione, the major intracellular antioxidant.
*GSH↑,
*HO-1↑, induction of Heme Oygenase-1 expression via NF-E2-related factor 2 activation may contribute to the cytoprotection exerted by fisetin against oxidative stress
*NRF2↑,
*ROS↓,
PI3K↓, Prostate: ↓ PI3-K (p85) expression [33] ↓ Akt phosphorylation at Ser473 & Thr308
Akt↓,
TumCCA↑, Induces cell cycle arrest in G1 phase ↓ cyclins D1, D2 and E ↓ cdks 2, 4
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
TumCMig↓, ↓ migration, invasion through MMP suppression
MMPs↓,
PSA↓, ↓ serum PSA levels
Dose↝, 30 mg synthetic genistein daily. Genistein at a dose that can be easily obtained from a diet rich in soy reduced the level of serum PSA in patients with localized CaP, without any effects on hormones. It was well tolerated and had a beneficial effect
PSA↓, Serum prostate specific antigen (PSA) decreased by 7.8% in the genistein arm and increased by 4.4% in the placebo arm
*LDL↓, Total cholesterol was significantly lower in the genistein arm (P = 0.013).
eff↑, Gold-silica nanoparticles designed to absorb near-infrared light at wavelengths of high tissue transparency provide a highly localized light-based strategy for the treatment of prostate cancer, with substantially reduced risks for deleterious treatme
PSA↓, Median prostate-specific antigen (PSA) at baseline decreased from 6.7 ng/mL at baseline to 3.9 ng/mL at 3 mo
*cardioP↑, Consumption of soy products have been linked to reduction in incidence or severity of chronic diseases such as cardiovascular, breast and prostate cancers, menopausal symptoms, bone loss, etc.
Risk↓, The antioxidant powers of isoflavones can reduce the long-term risk of cancer by preventing free radical damage to DNA. n Asian populations, where soy intake is high, the researchers found an inverse association between soy food intake and breast can
*BMD↑, isoflavones on BMD concluded that six month intake of soy isoflavones was adequate to exert a beneficial effect on it, especially of the lumber spine.
*eff↑, Maximal health benefits are most likely to be derived by consuming small amounts of isoflavone-rich foods throughout the day.
*antiOx↑, isoflavones have potent antioxidant properties, comparable to that of the well-known antioxidant vitamin E
*lipid-P↓, . The inhibition of lipid peroxidation, particularly of low density lipoprotein (LDL) by isoflavones may be an important mechanism by which they positively influence lipid profiles.
*LDL↓,
AntiThr↑, consumption of antioxidant/polyphenol rich foods might impart antithrombotic and cardiovascular protective effects via their inhibition of platelet hyperactivation or aggregation
AntiAg↑, Also, dietary isoflavones or polyphenols rich foods may substitute or complements currently used anti-platelet drugs in sedentary, obese, pre-diabetic or diabetic population
PSA↓, isoflavone supplementation appeared to slow the rising serum prostate specific antigen (PSA) concentration associated with prostate tumor growth of prostate cancer patients. However short-term intake of soy isoflavones did not affect PSA
TumCCA↑, Food intake rich with soy isoflavones may induce growth arrest and apoptosis of PCa
cognitive↑, healthy postmenopausal women with variable age groups receiving isoflavone tablets showed an increase in cognitive functions like working and visual memory
memory↑,
Dose↝, The supplement consisted of soy, isoflavones, lycopene, silymarin and antioxidants as main ingredients.
PSA↓, This translates into a 2.6 fold increase in the PSA doubling time from 445 to 1150 days for the supplement and placebo periods.
PSA↓, Nine patients (47%) experienced any PSA decline (mean decline 25.0%, range 2%-60%) by week 12.
toxicity↝, The most common adverse events were edema (52%), fatigue (38%), hypertension (24%), and hypokalemia (24%).
testos∅, Itraconazole modulates serum PSA levels without lowering serum testosterone.
toxicity↝, However, the magnitude of effect is modest, and treatment carries risk of toxicities associated with mineralocorticoid excess.
angioG↓, antifungal drug itraconazole inhibits angiogenesis and Hedgehog signaling and delays tumor growth in murine prostate cancer xenograft models.
HH↓,
Dose↝, 46 men with chemotherapy-naïve metastatic castration-resistant prostate cancer (CRPC) to receive low-dose (200 mg/day) or high-dose (600 mg/day) itraconazole until disease progression or unacceptable toxicity.
PSA↓, PSA response rates were 0% and 14.3%, respectively.
CTC↓, itraconazole had favorable effects on CTC counts, and it suppressed Hedgehog signaling in skin biopsy samples.
other↝, High-dose itraconazole (600 mg/day) has modest antitumor activity in men with metastatic CRPC that is not mediated by testosterone suppression.
toxicity↝, Adverse events were generally more frequent in the high-dose than in the low-dose arm (Table 2). Common toxicities in both arms included fatigue, pain, nausea and constipation.
*AntiFungal↑, Itraconazole is an FDA-approved antifungal drug used in the treatment of various mycoses that was repurposed as an antineoplastic agent after a screening effort identified that it could potently inhibit Hedgehog (Hh) pathway signaling in cancer.
antiNeop↑,
HH↓,
Dose↝, a phase II clinical trial suggested that itraconazole prescribed at high doses (600 mg per day) may have a role as an antineoplastic agent in men with metastatic castration-resistant prostate cancer (CRPC) who had not previously received chemotherapy
OS↑, In this trial, modest clinical activity using high-dose itraconazole in this setting was demonstrated as evidenced by longer PSA-progression-free survival and clinical/radiographic-progression-free survival compared to historical controls.
testos∅, Of note, treatment with itraconazole did not appear to have a significant effect on testosterone levels in these men with CRPC, suggesting that its clinical activity (unlike that of ketoconazole) may be independent of androgen modulation.
Dose↝, At initiation of treatment with itraconazole (300 mg, twice daily), the patient’s PSA level was 34.3 ng/mL and his testosterone level was in the non-castrate range
PSA↓, Following only one month of treatment with itraconazole, the PSA declined to 20.1 ng/mL, while the patient did report some grade-1 fatigue.
other↝, After 5 months of treatment, and despite a persistent PSA response with minimal adverse events, the patient developed asymptomatic hyperbilirubinemia necessitating discontinuation of itraconazole.
other↝, While the bilirubin level normalized after stopping itraconazole, this was accompanied by a subsequent increase in PSA level to 29.4 ng/mL, approximately one month after drug discontinuation.
HH↓, Inhibition of the Hedgehog pathway may mediate the clinical activity of itraconazole.
HH↓, Figure 1
angioG↓,
TumCCA↑,
MDR1↓,
P-gp/ABCB1↓,
mTOR↓,
VEGF↓,
Smo↓,
Gli1↓,
OS↑, Itraconazole 400 mg daily was administered over 4 days every 2 weeks. A response rate of 44% was achieved, with a higher median overall survival time (1,047 days) compared with that previously reported in other studies, which ranged between 7-10mts
PSA↓, After the patient declined castration treatment, itraconazole was administered and the PSA level reduced by >50% in 3 months (300 mg twice daily)
*BioAv↝, IVM’s distinct physicochemical profile, including high lipophilicity, poor aqueous solubility, and moderate acid stability, which collectively affect its bioavailability and pharmacokinetic behavior.
Apoptosis↑, induction of apoptosis, inhibition of tumor cell proliferation, and modulation of the tumor microenvironment across a range of malignancies.
TumCP↓,
Wnt↓, IVM inhibits the Wnt/β-catenin signaling pathway in gastric cancer cells, leading to suppressed tumor growth and metastasis.
β-catenin/ZEB1↓,
TumCG↓,
TumMeta↓,
PI3K↓, IVM disrupts the PI3K/AKT/mTOR pathway in pancreatic cancer, resulting in increased apoptosis and reduced cell proliferation.
Akt↓,
mTOR↓,
TumPF↓,
CSCs↓, IVM selectively suppresses CSCs in breast cancer models and downregulates genes associated with cellular stemness,
eff↑, combining IVM with immune checkpoint inhibitors, such as anti-PD1 antibodies, enhances antitumor immune responses and induces complete tumor regression in breast cancer models.
ChemoSen↑, Combination of Paclitaxel + Ivermectin or Paclitaxel + Pitavastatin produced maximum cytotoxicity and strong synergy in both chemoresistant lines, surpassing the effect of each drug alone
mtDam↑, IVM induces mitochondrial dysfunction (↓ψm, ↓ATP) with ↑ROS, inhibits NF-κB (↓p-p65), increases Bax/Bcl-2 and activates caspases 9/3
MMP↓,
ATP↓,
ROS↑,
NF-kB↓,
BAX↑,
Casp3↑,
Casp9↑,
ICD↑, induces immunogenic cell death
Ki-67↓, ↓Ki67, PSA
PSA↓,
YAP/TEAD↓, interferes with multiple oncogenic pathways, including WNT/TGF-β, PAK1/STAT3, YAP1, Akt/mTOR, and Wnt/β-catenin.
TumCG↓, juglone inhibited the growth of LNCaP cells in a dose-dependent manner.
MMP↓, loss of mitochondrial membrane potential, and caspase-3, -9 activation.
Casp3↑,
AR↓, Moreover, we found that juglone significantly inhibited the expression levels of androgen receptor (AR) and prostate-specific antigen (PSA
PSA↓,
Casp3↑, In LNCaP cells, it triggered apoptosis through the intrinsic pathway, promoting the activation of caspases 3 and 9, and decreasing mitochondrial potential (ΔΨ)
Casp9↑,
MMP↓,
AR↓, At sub-toxic concentrations, it downregulated ARs and PSA expression
PSA↓,
E-cadherin↑, Juglone upregulated the expression of the epithelial marker E-cadherin while reducing the mesenchymal factors N-caderin and vimentin.
N-cadherin↓,
Vim↓,
Akt↓, Furthermore, it synergistically inhibited the Akt/glycogen synthase kinase-3β (GSK-3β)/Snail axis that would physiologically promote E-cadherin repression and EMT induction
GSK‐3β↓,
EMT↑,
TumCI↓, decreased cell invasions by 56% and 80%, respectively, on BxPC-3 and PANC-1 cell lines.
MMP9↓, Juglone significantly dropped the protein level of MMP-9 and the vascular endothelial growth factor (VEGF) reporter Phactr-1 in both cell lines, while a drop of MMP-2 was evident only on BxPC-3
VEGF↓,
MMP2↓,
TumCCA↑, juglone promoted G1 cell-cycle arrest [94,95] and ROS-driven apoptosis
ROS↑,
Apoptosis↑,
GSH↓, Glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase protein levels diminished
Catalase↓,
SOD↓,
GPx↓,
DNAdam↑, juglone cytotoxicity is, at least partially, ascribed to DNA damage
γH2AX↑, high levels of γ-H2AX were registered when juglone was tested in combination with ascorbate.
eff↑, juglone’s anticancer profile (in terms of proliferation inhibition, cytotoxicity, and ROS induction) was highly improved by ascorbate [115], revealing an interesting synergistic activity between these two compounds
BAX↑, upregulation of many proteins involved in the intrinsic and extrinsic pathway, such as Bax, Cyt-c, Fas cell surface death receptor (Fas), Fas-ligand.
Fas↑,
Pin1↓, On U251 glioblastoma cells, juglone arrested cell growth by promoting apoptosis with the involvement of peptidyl-prolyl cis/trans isomerase (Pin1) inhibition [111]. Juglone is a well-known Pin1 inhibitor
*antiAll↑, Lambertianic acid (LA) is known to have anti-allergic and antibacterial effects
*Bacteria↓,
AR↓, LA decreased not only AR protein levels, but also cellular and secretory levels of PSA.
PSA↓,
TumCCA↑, LA suppressed cell proliferation by inducing G1 arrest, downregulating CDK4/6 and cyclin D1 and activating p53 and its downstream molecules, p21 and p27.
CDK4↓,
CDK6↓,
cycD1/CCND1↓,
P53↑,
P21↑,
p27/CDKN1B↓,
Apoptosis↑, LA induced apoptosis and the expression of related proteins, including cleaved caspase-9 and -3, c-PARP and BAX, and inhibited BCl-2.
cl‑Casp9↑,
cl‑Casp3↑,
cl‑PARP↑,
BAX↑,
Bcl-2↓,
Dose↝, LA decreased the number of LNCaP cells concentration and time dependently (IC50 109 μM).
*Obesity↓, potential health benefits in attenuating obesity, allergies and different cancers including breast, liver, lung and prostate cancer.
*AntiCan↑,
*AMPK↑, rats with high fat diet (HFD)-induced obesity by activating adenosine monophosphate activated protein kinase (AMPK)
*β-HEX↓, it was also observed that LA can suppress the release of β-hexosaminidase in a concentration-independent manner in BMMC
NA↑, anti-allergic activity
TumCCA↑, LA-treated MDA-MB-231 cells revealed that LA induces G2/ M phase arrest
AMPK↑, , LA activates AMPK and acetyl-CoA carboxylase (ACC) through phosphorylation and can suppress protein kinase B (AKT) phosphorylation,
ACC↑,
p‑Akt↓,
FOXM1↓, LA actively attenuates the expression of forkhead box protein M1 (FOXM1) and its regulated gene products, including proliferative proteins (Cyclin B1) and anti-apoptotic proteins (X-linked inhibitor of apoptosis protein [XIAP] and B-cell lymphoma 2 [
CycB/CCNB1↓,
XIAP↓,
Bcl-2↓,
p‑STAT3↓, LA suppresses the phosphorylation of STAT3 and NF-κB, the expression of p300 and RelA/ p65 acetylation,
p‑NF-kB↓,
Bcl-xL↓, LA blocks the expression of NF-κB regulated genes, including anti-apoptotic proteins (Bcl-2, Bcl-xL, XIAP and survivin), angiogenic protein vascular endothelial growth factor (VEGF), inflammatory protein COX-2, oncogenic genes cellular myelocytomato
survivin↓,
VEGF↓,
COX2/PTGS2↓,
cMyc↓,
IL6↓, and inflammatory mediators IL-6 and tumour necrosis factor-alpha (TNF-α) in the MCF-7 cells
TNF-α↓,
ROS↑, LA exhibits anticancer effects on hepatocellular carcinoma cells (HCC) through induction of apoptotic pathway by ROS-dependent activation of liver kinase B1 (LKB1)/AMPK/ ACC signalling cascades
STK11/LKB1↑,
cl‑Casp3↑, it induces the cleavage of caspase-3 and PARP along with the suppression of antiapoptotic proteins, Bcl-2 and Bcl-xl.
cl‑PARP↑,
eff↑, LA (20 μM) together with TRAIL (20 ng/ml) shows significant cytocidal effects in TRAIL resistant nonsmall cell lung cancer cell
AR↓, LA exerts anticancer effects by suppressing AR pathway in AR-sensitive prostate cancer cells LNCaP.
TumCP↓, 24 h LA treatment downregulates cell proliferation by reducing several protein levels, including p-53, p-p53, p21, p27, cyclin D1 and cell division kinase 4 (CDK4).
p‑P53↓,
P21↓,
p27/CDKN1B↓,
cycD1/CCND1↓,
CDK4↓,
PSA↓, LA exhibits anticancer properties by inhibiting AR expression and PSA in cellular and secretory levels
STAT3↓, LA induces apoptosis via miRNA-134 mediated inhibition of STAT3 and RelA/p65 acetylation
ac‑p65↓,
*antiAll↑, In conclusion, LA could be utilized in treating allergies, obesity and different cancers.
eff↑, Our study shows that lycopene supplementation does not modify the main hallmarks of cancer, but it increases circulating lycopene concentration in patients under cancer therapy, which could have a positive impact on potential clinical and molecular o
cardioP↑, A systematic review and meta-analysis reported that tomato and lycopene supplementation have positive effects on cardiovascular risk factors
eff?, lycopene supplementation may have benefits in the oncology population during cancer treatment.
PSA↓, Lycopene supplementation improved PSA levels in patients with an intermediate risk of cancer
RenoP↑, Surprisingly, lycopene has been shown to improve renal makers of nephrotoxicity after cisplatin treatment
Risk↓, Dietary intake of lycopene and soy has been associated with a lower risk of prostate cancer
PSA↓, In a previous Phase II clinical trial in prostate cancer patients, we observed prostate-specific antigen (PSA) stabilization with soy isoflavone intake
Dose↝, randomly assigned to receive a tomato extract capsule containing 15 mg of lycopene alone (n = 38) or together with a capsule containing 40 mg of a soy isoflavone mixture (n = 33) twice daily orally for a maximum of 6 mo.
eff↝, However, 35 of 37 (95%) evaluable patients in the lycopene group and 22 of 33 (67%) evaluable patients in the lycopene plus soy isoflavone group achieved stable disease described as stabilization in serum PSA level.
TumCP↓, Lycopene suppress the progression and proliferation
TumCCA↑, Lycopene has been found to effectively suppress the progression and proliferation, arrest in-cell cycle, and induce apoptosis of prostate cancer cells in both in-vivo and in-vitro conditions.
Apoptosis↑,
*neuroP↑, the neuro-protective effect of lycopene, mediates the signaling pathways, by inhibiting NF-κB (nuclear factor-κB) and JNK protein (c-Jun N-terminal kinase), and activating Nrf2 (Nuclear factor erythroid 2-related factor 2) and BDNF (
*NF-kB↓,
*JNK↓,
*NRF2↑,
*BDNF↑,
*Ca+2↝, as well as keeping homeostasis by restoring intracellular Ca2+
*antiOx↑, most powerful and natural antioxidants, and its role in preventing prostate cancer.
*AntiCan↑,
*Inflam↓, Anti-inflammatory properties of lycopene depends on time, and it has been found to be through the decrease of inflammatory cytokines (i.e. IL1, IL6, IL8 and tumor necrosis factor-α (TNF-α)
*IL1↓,
*IL6↓,
*IL8↓,
*TNF-α↓,
NF-kB↓, lycopene increased the expression of BCO2 enzyme in an androgen-sensitive cell line that prevented cancer cell proliferation and reduced the NF-κB activity
DNAdam↓, 20 and 50 μM doses of lycopene had an effect on PC3 and DU145 cell lines in inducing apoptosis with DNA damages, and preventing cell growth and colony formation
PSA↓, lycopene twice a day for 3 weeks, showed that lycopene decreases the risk and growth of prostate cancer cells, and also a decrease in the level of PSA,
P53↓, down-regulation of p53, Cyclin-D1, and Nrf-2 have occurred after the incubation of prostate cancer cells with the lycopene received patient’s sera in comparison with placebo
cycD1/CCND1↓,
NRF2↓,
Akt2↓, treatment with lycopene in PC3 cancer cell lines was associated with down-regulation of AKT2 [
PPARγ↓, Another anti-proliferative effect of lycopene was done by increasing PPARγ-LXRα-ABCA1signaling molecules in protein and mRNA level
*eff↑, Among groups, all parameters showed highly significant differences in favor of Group A. (PEMF)
*eff↑, Pelvic floor exercises deliver distinctive unmistakable effects on the prostate, particularly in individuals who present with BPH
*BloodF↑, Exercise can enhance blood circulation to the pelvic region, enabling the body to actively eliminate harmful agents and waste products;
*Diff↝, EMF is thought to have the ability to affect the cells that induce different cellular changes including cell reproduction and differentiation
*Dose↝, EMF device (PMT-120 Desktop, ElectroMeds, USA) was worked with impact to patient with damped trains of magnetic oscillations with a period of 20–1,100 nanoseconds and an intensity of 0.12–18 microtesla
*Dose↝, and a decreased damping of at least 0.05 and a repetition rate between the trains in the range of 25–30 Hz.
*Dose↝, application was directed to the perineum with the patient lying in the lateral recumbent position.
*Dose↝, 30 minutes for each day, five times each week for 4 progressive weeks.
*Dose↝, Aerobic exercises: regular aerobic exercise for 20–60 minutes undertaken five times each week at 55–90% of the maximal heart rate is estimated as 220 −age in years.
*Dose↝, pelvic floor exercises to be performed in daily sessions in lying, sitting, and standing positions consisting of 10 seconds of contractions followed by 10 seconds of relaxation and repeating the exercises 15 times each session.
*Dose↝, While, fast twitch muscle fibers can be trained through asking the patient to contract as if he controls his urine by quick contraction and relaxation of the levator ani muscles 20 times, rest for ten seconds, and then repeat again for a total of 2 t
*UFR↑, RU: post void residual urine volume, FR: urine flow rate, PSA: Intragroup comparisons showed a significant difference (p<0.05) in Groups A and B in all parameters
*UR↓,
*PSA↓,
*other↑, The results of the current study demonstrated that the use of PEMF and exercise therapy is beneficial in the treatment of BPH.
*Inflam↓, The anti-inflammatory capacity of PEMF should additionally be granted16)
*Inflam↓, OC exhibits promising therapeutic potential against both inflammation and cancer.
AntiCan↑,
*COX2/PTGS2↓, OC was able to inhibit the enzymaticactivity of cyclooxigenease-2 (COX-1) and cyclooxigenease-2 (COX-2) with greater potencycompared to ibuprofen
*ROS↓, figure 3
*TNF-α↓,
*IL1β↓,
*iNOS↓,
TumCP↓, OC also effectively reduces cell proliferation and limits the production of the extracellular matrix in LX2 cells, suggesting its antifibrotic properties
*AntiAg↑, Healthy men: Anti-platelet effects
mTOR↓, Oleocanthalhas exhibited robust anti-proliferative effects in multiple breast cancer cell lines, accompanied by the downregulation of phosphorylated mTOR
STAT3↓, OC was shown to suppress STAT3 activity
ERK↓, OC was able to inhibit ERK1/2 and AKT phosphorylation and downregulate Bcl-2expression
p‑Akt↓,
Bcl-2↓,
ROS↑, OC effectively impeded the formation of cell colonies, triggered apoptosis, and incited the generation of intracellular ROS within cancer cells.
PSA↓, ↓PSA levels in mouse model
CycB/CCNB1↓, quercetin has a role in the reduction of cyclin B1 and CDK1 levels,
CDK1↓,
EMT↓, quercetin suppresses epithelial to mesenchymal transition (EMT) and cell proliferation through modulation of Sonic Hedgehog signaling pathway
PI3K↓, Inhibitory effects of quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
MAPK↓,
Wnt/(β-catenin)↓, wnt
PSA↓,
VEGF↓,
PARP↑,
Casp3↑,
Casp9↑,
DR5↑,
ROS⇅,
Shh↓,
P53↑, figure 1
P21↑, quercetin regulates p21 expression
EGFR↓,
TumCCA↑, quercetin has cell-specific anti-proliferative impacts via stimulation of cell cycle arrest at the G1 stage.
ROS↑, quercetin has been shown to suppress carcinogenesis through various mechanisms including affecting cell proliferation, production of reactive oxygen species and expression of miR-21
miR-21↓,
TumCP↓,
selectivity↑, In breast cancer cells, quercetin inhibits cell proliferation without exerting any cytotoxic impact on normal breast epithelium
PDGF↓, figure 1
EGF↓,
TNF-α↓,
VEGFR2/KDR/Flk1↓,
mTOR↓,
cMyc↓,
MMPs↓,
GRP78/BiP↑,
CHOP/DDIT3↑,
| - |
in-vitro, |
Pca, |
LNCaP |
|
|
|
- |
in-vitro, |
Pca, |
LAPC-4 |
|
|
|
PSA↓, quercetin inhibited the secretion of the prostate-specific, androgen-regulated tumor markers, PSA and hK2
AR↓, Quercetin inhibits the expression of AR protein
NKX3.1↓, Quercetin can also significantly down-regulate the expression of another prostate-specific gene, NKX3.1,
HK2↓, Quercetin inhibits PSA and hK2 secretion
AR↓,
PI3K/Akt↓, The combination treatment significantly inhibited both AR and PI3K/Akt pathways compared to control.
miR-21↓,
STAT3↓,
BAD↓,
PRAS40↓,
GSK‐3β↓,
PSA↓,
NKX3.1↑,
Bax:Bcl2↑, a significantly increased ratio of Bax to Bcl-2 protein expression was observed in LAPC-4 cells by the combination treatment compared to Q alone, and a trend to increase in LNCaP cells
miR-19b↓,
miR-148a↓,
AMPKα↓,
TumCP↓, The anti-proliferative activity of arctigenin was 10-20 fold stronger than quercetin in both cell lines.
chemoPv↑, combination of arctigenin and quercetin, that target similar pathways, at low physiological doses, provides a novel regimen with enhanced chemoprevention in prostate cancer.
TumCMig↓, Enhanced inhibition of cell migration
| - |
in-vitro, |
Pca, |
HEK293 |
|
|
|
- |
in-vitro, |
NA, |
22Rv1 |
|
|
|
- |
in-vitro, |
NA, |
C4-2B |
|
|
|
hnRNPA1↓, quercetin downregulates hnRNPA1 expression
PSA↓,
NKX3.1↓,
FKBP5↓,
UBE2C↓,
AR-FL↓, FL AR
AR-V7↑, downregulates the expression of AR-V7, antagonizes androgen receptor signaling
AR↓, Quercetin downregulates androgen receptor signaling
eff↑, Quercetin resensitizes enzalutamide-resistant xenografts to enzalutamide in vivo
TumVol↓,
BioAv↓, The bioavailability of quercetin is low as it is present in glycosylated form, which can be readily metabolized by enzymes in the gut and liver, leading to low systemic concentrations in the body
BioAv↓, Resveratrol is poorly bioavailable, and that considered the major hindrance to exert its therapeutic effect, especially for cancer management
BioAv↓, at lower doses (25 mg per healthy subject) demonstrate that the mean proportion of free resveratrol in plasma was 1.7–1.9% with a mean plasma concentration of free resveratrol around 20 nM
Dose↑, Boocock and his colleagues studied the pharmacokinetic of resveratrol; in vitro data showed that minimum of 5 µmol/L resveratrol is essential for the chemopreventive effects to be elicited
eff↑, Despite the low bioavailability of resveratrol, it shows efficacy in vivo. This may be due to the conversion of both glucuronides and sulfate back to resveratrol in target organs such as the liver
eff↑, repeated administration of high doses of resveratrol generates a higher plasma concentration of parent and a much higher concentration of sulfate and glucuronide conjugates in the plasma
Dose↑, The doses tested in this study were 0.5, 1.0, 2.5 or 5.0 g daily for 29 days. No toxicity was detected, but moderate gastrointestinal symptoms were reported for 2.5 and 5.0 g doses
BioAv↑, the co-administration of piperine with resveratrol was used to enhance resveratrol bioavailability
ROS↑, Recent studies have shown that resveratrol increases ROS generation and decreases mitochondrial membrane potential
MMP↓,
P21↑, treatment decreased the viability of melanoma cells by activating the expression of both p21 and p27, which promoted cell cycle arrest.
p27/CDKN1B↑,
TumCCA↑,
ChemoSen↑, Additionally, the use of resveratrol with cisplatin in malignant human mesothelioma cells (MSTO-211H and H-2452 cells) synergistically induces cell death by increasing the intracellular ROS level [64].
COX2/PTGS2↓, covers the down-regulation of the products of the following genes, COX-2, 5-LOX, VEGF, IL-1, IL-6, IL-8, AR and PSA [93].
5LO↓,
VEGF↓,
IL1↓,
IL6↓,
IL8↓,
AR↓,
PSA↓,
MAPK↓, by preventing also the activation of the MAPK and PI3K/Akt signaling pathways, it suppresses HIF-1a and VEGF release in ovarian cancer cells of humans
Hif1a↓,
Glycolysis↓, Resveratrol was found to effectively impede the activation, invasion, migration and glycolysis of PSCs induced by reactive oxygen species (ROS) by down-regulating the expression of microRNA 21 (miR-21)
miR-21↓,
PTEN↑, also by increasing the phosphatise and tensin homolog (PTEN) protein levels
Half-Life↝, 25 mg/70 kg resveratrol administered to healthy human participants, the compound predominantly appeared in the form of glucuronide and sulfate conjugates in serum and urine and reached its peak concentrations in serum about 30 min after ingestion
*IGF-1↓, Brown and colleagues noted how a major decline in circulating insulin-like growth factor (IGF)-I as well as IGF-binding proteins (IGFBP-3) among healthy individuals can be credited to the intake of resveratrol
*IGFBP3↑,
Half-Life↓, Microactive® and Resveratrol SR and manufactured by Bioactives. This compound is capable of sustained release for over 12 h to increase intestinal residence time.
*Inflam↓, Resveratrol is known to have potent anti-inflammatory and anti-oxidant effects and to inhibit platelet aggregation and the growth of a variety of cancer cells.
*antiOx↑,
*AntiAg↑,
*chemoPv↑, Its potential chemopreventive and chemotherapeutic activities have been demonstrated in all three stages of carcinogenesis
ChemoSen↑,
BioAv↑, Compared to other known polyphenols, such as quercetin and catechin, trans-resveratrol is well absorbed much more efficiently following oral administration to humans
Half-Life↝, Compared to resveratrol, which has a plasma half-life of 8–14 min, the metabolites have a plasma half-life of about 9.2 hours
COX2/PTGS2↓, there was inhibited expression of anti-apoptotic proteins, such as survivin, and markers of tumor promotion, cyclooxygenase (COX)-2, and ornithine decarboxylase (ODC) were observed
cycD1/CCND1↓, Resveratrol decreased the expression of cyclins D1 and D2, Cdk 2, 4 and 6, and proliferating cell nuclear antigen (PCNA) whereas p21WAF1/CIP1 was increased
CDK2↓,
CDK4↓,
CDK6↓,
P21↑,
MMP9↓, associated with decreased COX-2 and matrix metalloprotease-9 expression and suppression of NFκB activation
NF-kB↓,
Telomerase↓, Relatively high concentrations also substantially downregulate telomerase activity
PSA↓, Resveratrol downregulates PSA by a mechanism independent of changes in AR
MAPK↑, Resveratrol treatment of various prostate cells also accompanied the activation of MAPK signaling and an increase in cellular p53
P53↑,
TumCG↓, SW480 colon cancer cells and found RE to significantly decrease cell growth at a concentration of 31.25 µg/mL (48 h),
TumCP↓, Cell proliferation was dramatically decreased and cell cycle arrest was induced in HT-29 and SW480 c
TumCCA↑,
ChemoSen↑, RE enhanced the inhibitory effects of the chemotherapeutic drug 5-fluorouracil (5-FU) on proliferation and sensitized 5-FU resistant cells
NRF2↑, HCT116 ↑ Nrf2, ↑ PERK, ↑ sestrin-2, ↑ HO-1, ↑ cleaved-casp 3
PERK↑,
SESN2↑,
HO-1↑,
cl‑Casp3↑,
ROS↑, HT-29 ↑ ROS accumulation, ↑ UPR, ↑ ER-stress
UPR↑,
ER Stress↑,
CHOP/DDIT3↑, HT-29: ↑ ROS levels, ↑ HO-1 and CHOP
HER2/EBBR2↓, SK-BR-3: ↑ FOS levels, ↑ PARP cleavage, ↓ HER2, ↓ ERBB2, ↓ ERα receptor.
ER-α36↓,
PSA↓, LNCaP : ↑ CHOP, ↓ PSA production, ↑ Bax, ↑ cleaved-casp 3, ↓ androgen receptor expression
BAX↑,
AR↓,
P-gp/ABCB1↓, A2780: ↓ P-glyco protein, ↑ cytochrome c gene, ↑ hsp70 gene
Cyt‑c↑,
HSP70/HSPA5↑,
eff↑, This study noted that the rosemary essential oil was more potent than its individual components (α-pinene, β-pinene, 1,8-cineole) when tested alone at the same concentrations.
p‑Akt↓, A549: ↓ p-Akt, ↓ p-mTOR, ↓ p-P70S6K, ↑ PARP cleavage
p‑mTOR↓,
p‑P70S6K↓,
cl‑PARP↑,
eff↑, RE containing 10 µM equivalent of CA, or 10 µM CA alone (96 h) potentiated the ability of vitamin D derivatives to inhibit cell viability and proliferation, induce apoptosis and cell cycle arrest and increase differentiation of WEHI-3BD murine leukem
Showing Research Papers: 1 to 50 of 58
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Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
NA↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
ARE/EpRE↑, 1, Catalase↓, 2, GPx↓, 1, GSH↓, 2, HO-1↑, 1, ICD↑, 1, MDA↑, 1, NRF2↓, 1, NRF2↑, 2, ROS↑, 10, ROS⇅, 1, SAM-e↝, 1, SOD↓, 2,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, EGF↓, 1, p‑MEK↓, 1, MMP↓, 4, mtDam↑, 1, XIAP↓, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACC↑, 1, AMPK↑, 2, cMyc↓, 3, CYP3A4↓, 1, FASN↓, 1, Glycolysis↓, 1, HK2↓, 2, LAT↓, 1, NAD↝, 1, PI3K/Akt↓, 1, PI3K/Akt↝, 1, PPARγ↓, 1, PSMB5↓, 1, STK11/LKB1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 4, p‑Akt↓, 4, APAF1↑, 1, Apoptosis↑, 5, BAD↓, 1, BAX↑, 6, Bax:Bcl2↑, 2, Bcl-2↓, 5, Bcl-xL↓, 2, BID↑, 1, Casp↑, 1, Casp3↑, 5, cl‑Casp3↑, 5, cl‑Casp7↑, 1, cl‑Casp8↑, 1, Casp9↑, 4, cl‑Casp9↑, 2, CK2↓, 2, Cyt‑c↑, 3, DR5↑, 1, Fas↑, 1, cl‑IAP2/BIRC3↑, 1, p‑JNK↓, 1, MAPK↓, 2, MAPK↑, 1, MAPK↝, 1, p27/CDKN1B↓, 2, p27/CDKN1B↑, 1, Proteasome↓, 1, survivin↓, 1, Telomerase↓, 2, YAP/TEAD↓, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
AMPKα↓, 1, HER2/EBBR2↓, 2, Sp1/3/4↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1, miR-21↓, 3, other↑, 1, other↝, 3, p‑pRB↓, 1, tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ATF6↑, 1, CHOP/DDIT3↑, 2, eIF2α↑, 1, ER Stress↑, 1, GRP78/BiP↑, 1, HSP70/HSPA5↑, 1, HSPs↓, 1, PERK↑, 1, UPR↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
SESN2↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1, DNAdam↑, 1, NKX3.1↓, 2, NKX3.1↑, 1, P53↓, 2, P53↑, 4, p‑P53↓, 1, PARP↑, 1, cl‑PARP↑, 4, PARP1↑, 1, γH2AX↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 2, CDK2↓, 3, CDK4↓, 5, Cyc↓, 2, CycB/CCNB1↓, 2, cycD1/CCND1↓, 7, cycE/CCNE↓, 2, P21↓, 2, P21↑, 7, Securin↓, 1, TumCCA↑, 12,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
AR-FL↓, 1, AR-V7↑, 1, BRAF↝, 1, CSCs↓, 1, EMT↓, 1, EMT↑, 1, ERK↓, 2, p‑ERK↓, 1, FOXM1↓, 1, Gli1↓, 1, GSK‐3β↓, 2, p‑GSK‐3β↓, 1, HDAC↓, 1, HH↓, 4, IGF-1↓, 7, IGFBP3↑, 1, mTOR↓, 5, p‑mTOR↓, 1, p‑P70S6K↓, 1, PI3K↓, 4, PTEN↑, 2, PTEN↝, 1, Shh↓, 1, Smo↓, 1, STAT3↓, 3, p‑STAT3↓, 1, TCF↓, 1, TumCG↓, 5, Wnt↓, 2, Wnt/(β-catenin)↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, Akt2↓, 1, AntiAg↑, 2, Ca+2↓, 1, Ca+2↑, 1, cal2↑, 1, Cdc42↓, 1, CDK4/6↓, 1, E-cadherin↑, 3, ER-α36↓, 1, FAK↓, 1, hnRNPA1↓, 1, ITGB4↓, 1, Ki-67↓, 1, miR-148a↓, 1, miR-19b↓, 1, MMP1↓, 1, MMP2↓, 1, MMP7↓, 1, MMP9↓, 2, MMPs↓, 3, N-cadherin↓, 2, PDGF↓, 1, Rho↓, 1, serineP↓, 1, TGF-β↓, 1, TumCI↓, 2, TumCMig↓, 3, TumCP↓, 9, TumMeta↓, 3, TumPF↓, 1, uPA↓, 1, Vim↓, 1, β-catenin/ZEB1↓, 3,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 4, ATF4↑, 1, EGFR↓, 3, HIF-1↓, 1, Hif1a↓, 2, VEGF↓, 7, VEGFR2/KDR/Flk1↓, 1,
Barriers & Transport(tgid=15) ⓘ
P-gp/ABCB1↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 4, IL1↓, 2, IL6↓, 3, IL8↓, 1, Neut↑, 1, NF-kB↓, 5, p‑NF-kB↓, 1, ac‑p65↓, 1, PGE2↓, 1, PSA↓, 49, TNF-α↓, 3,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
AR↓, 18, CDK6↓, 2, FKBP5↓, 1, testos∅, 2,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 3, BioAv↑, 3, ChemoSen↑, 6, Dose↑, 3, Dose↝, 10, eff?, 1, eff↑, 15, eff↝, 1, eff∅, 1, Half-Life↓, 1, Half-Life↑, 1, Half-Life↝, 2, MDR1↓, 1, RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
AR↓, 18, BMPs↑, 1, BRAF↝, 1, CTC↓, 1, EGFR↓, 3, FOXM1↓, 1, HER2/EBBR2↓, 2, IL6↓, 3, Ki-67↓, 1, PSA↓, 49,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 3, antiNeop↑, 1, cardioP↑, 1, chemoP↑, 1, chemoPv↑, 2, cognitive↑, 1, memory↑, 1, OS↑, 3, Pin1↓, 1, PRAS40↓, 1, RenoP↑, 1, Risk↓, 4, Risk↝, 1, toxicity↝, 3, TumVol↓, 7, UBE2C↓, 1,
Total Targets: 235
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
antiAll↑, 2, UFR↑, 1, UR↓, 1, β-HEX↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 6, Catalase↑, 1, GPx↑, 1, GSH↑, 3, HO-1↑, 2, lipid-P↓, 2, NRF2↑, 3, ROS↓, 2, SAM-e↑, 1, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↝, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, p‑CREB↑, 1, LDL↓, 2, NAD↝, 1,
Cell Death(tgid=5) ⓘ
iNOS↓, 1, JNK↓, 1, MAPK↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
Diff↝, 1, ERK↑, 1, IGF-1↓, 1, IGFBP3↑, 1,
Migration(tgid=13) ⓘ
5LO↓, 3, AntiAg↑, 2, Ca+2↝, 2, PKCδ↓, 1, serineP↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 2, IL1↓, 1, IL1β↓, 1, IL6↓, 1, IL8↓, 1, Inflam↓, 9, NF-kB↓, 3, PGE2↓, 1, PSA↓, 1, TNF-α↓, 3, VitD↑, 2,
Synaptic & Neurotransmission(tgid=18) ⓘ
BDNF↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
testos↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↝, 1, Dose↑, 1, Dose↝, 8, eff↑, 5, Half-Life↝, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
BloodF↑, 1, BMD↑, 2, BMPs↑, 1, Calcium↑, 2, hs-CRP↓, 1, IL6↓, 1, Mag↑, 2, PSA↓, 1, VitD↑, 2,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 2, cardioP↑, 1, chemoP↑, 1, chemoPv↑, 3, ChemoSideEff↓, 1, cognitive↑, 2, memory↓, 1, memory↑, 3, motorD↓, 1, neuroP↑, 3, Obesity↓, 1, Risk↓, 1, toxicity↓, 2,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, Bacteria↓, 1,
Total Targets: 75
Scientific Paper Hit Count for: PSA, prostate-specific antigen
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:264 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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