AntiTum Cancer Research Results

AntiTum, AntiTumor: Click to Expand ⟱
Source:
Type:
AntiTumor


Scientific Papers found: Click to Expand⟱
5874- CA,    Carnosic Acid Mediates Production of Reactive Oxygen Species to Regulate Mitogen-Activated Protein Kinase Pathway Phosphorylation and Induce Apoptosis in Human Breast Cancer Cells
- vitro+vivo, BC, T47D - in-vitro, BC, MCF10
AntiTum↓, Carnosic acid (CA) exerts an anti‐tumor effect via generating ROS or activating the mitochondria‐related apoptosis pathway in vitro and in vivo.
ROS↑, CA promoted cancer cell apoptosis via ROS generation, which activated c‐Jun N‐terminal kinase (JNK) and p38 phosphorylation.
cJun↑, CA Activated JNK and p38 in Breast Cancer Cell Lines
p‑p38↑,
Apoptosis↑, CA induced apoptosis of hepatocellular carcinoma cells via the reactive oxygen species (ROS)‐mediated mitochondrial pathway
ROS↑,
eff↑, Furthermore, the combined application of CA and curcumin suppressed the proliferative activity and disrupted the mitochondrial function of metastatic prostate cancer cells compared with their individual uses
TumCP↓, CA Inhibited Breast Cancer Proliferation and Glucose Uptake
glucose↓, Glucose consumption was accelerated by low concentrations of CA, but decreased with increasing time and CA concentration.
BAX↑, up‐regulating Bax and PARP and down‐regulating Bcl‐2.
PARP↑,
Bcl-2↓,
eff↓, We then abrogated the effect of CA‐induced ROS using the antioxidant NAC (5 mM).
Ki-67↓, These findings indicated that CA could accelerate tumor apoptosis by up‐regulating Bax expression and down‐regulating Ki67 and Bcl‐2 in vivo.
toxicity↝, Furthermore, CA did not injure vital organs.
STAT3↓, CA has been reported to suppress the STAT3 signaling pathway through ROS generation and inhibit the phosphoinositide 3‐kinase/Akt/mTOR signaling pathway in colon cancer and lung cancer
PI3K↓,
Akt↓,
mTOR↓,

6214- CUR,    Curcumin Nanoparticles-related Non-invasive Tumor Therapy, and Cardiotoxicity Relieve
TumCD↓, Curcumin plays the antitumor effect by directly promoting tumor cell death and reducing tumor cells' invasive ability.
TumCI↓,
*Inflam↓, curcumin has many pharmacological effects, such as anti-inflammation, antioxidation, antitumor, etc.
*antiOx↓,
*AntiTum↓,
NF-kB↓, Curcumin exerts the therapeutic effect mainly by inhibiting the nuclear factor-κB (NF-κB) signal pathway, inhibiting the production of cyclooxygenase-2 (COX-2),
COX2/PTGS2↓,
Casp9↓, promoting the expression of caspase-9, and directly inducing reactive oxygen species (ROS) production in tumor cells.
ROS↑, Curcumin can induce lethal levels of reactive oxygen species (ROS) in tumors
BioAv↑, Curcumin nanoparticles can solve curcumin's shortcomings, such as poor water solubility and high metabolic rate, and can be effectively used in antitumor therapy.
RadioS↑, Figure 1, Curcumin Increases Radiosensitivity of Tumor
ChemoSen↑,
Imm↑,
PhotoS↑, Curcumin Mediates the Antitumor Effect of PDT
sonoS↑, Curcumin Mediates the Antitumor Effect of SDT
5LO↓, down-regulating the activities of cyclooxygenase-2 (COX-2), lipoxygenase (LOX), inducible nitric oxide synthase (iNOS) and so on, reducing the production of proinflammatory cytokines such as IL-2, tumor necrotic factor-α (TNF-α),
iNOS↓,
IL2↓,
TNF-α↓,
Casp9↑, activating intracellular caspase-9 and caspase-3, reducing the expression of p53, inhibiting Bcl2, and promoting the expression of Bax and down-regulating the proportion of Bcl2/Bax
Casp3↑,
Bcl-2↓,
BAX↑,
Apoptosis↑, promote apoptosis by activating caspase-4 and stimulating the Endoplasmic reticulum (ER) stress pathway and mitochondria stress pathway in tumor cells [
ER Stress↑,
cycD1/CCND1↓, It reduces the expression of cyclin D1, cyclin kinase-dependent kinase 2 (CDK2), cdc2/cyclin B complex, and other cell cycle-related proteins,
CDK2↓,
CycB/CCNB1↓,
TumCCA↑, blocks tumor cells from G1 / S phase and G2 / M phase, thus exerting an antitumor effect
MMPs↓, curcumin inhibits tumor invasion and metastasis by inhibiting NF-κB and other signaling pathways, such as chemokine and matrix metalloproteinases (MMPs)
*radioP↑, Curcumin can effectively treat and prevent radiation adverse reactions such as radiation dermatitis and radiation pneumonia by reducing the expression of inflammatory factors such as fibrotic cytokines, TNF-α, and IL-1, inhibiting NF-κB signal pathwa
chemoP↑, Protective Effect of Curcumin on Side Effects of Chemotherapy
hepatoP↑, urcumin alleviates the hepatotoxicity caused by chemotherapy through anti-inflammation and antioxidation, reducing the level of liver fibrosis and blood lipids [
cardioP↑, Using curcumin to reduce the cardiotoxicity of chemotherapy can improve the therapeutic effect of tumors and patients' prognosis and quality of life.
eff↑, Curcumin Enhances the Therapeutic Effect of Immunotherapy
PhotoS↑, it has the potential to be a new photosensitizer
eff↑, Curcumin nanoparticles with functions of relieving hypoxia and consuming GSH could improve the ability of curcumin to induce ROS and promote ROS- mediated tumor cell death
ROS↑,
GSH↓,

1843- dietFMD,  BTZ,    Cyclic Fasting–Mimicking Diet Plus Bortezomib and Rituximab Is an Effective Treatment for Chronic Lymphocytic Leukemia
- in-vivo, CLL, NA
AntiTum↓, Cyclic fasting–mimicking diet (FMD) is an experimental nutritional intervention with potent antitumor activity in preclinical models of solid malignancies.
Apoptosis↑, murine CLL models had mild cytotoxic effects, which resulted in apoptosis activation mediated in part by lowered insulin and IGF1 concentrations.
IGF-1↓,
eff↑, In CLL cells, fasting conditions promoted an increase in proteasome activity that served as a starvation escape pathway. Pharmacologic inhibition of this escape mechanism with the proteasome inhibitor bortezomib resulted in a strong enhancement
OS↑, combining cyclic fasting/FMD with bortezomib and rituximab, an anti-CD20 antibody, delayed CLL progression and resulted in significant prolongation of mouse survival
eff↑, recent clinical reports have shown that combining cyclic FMD with chemotherapy, endocrine therapies, or immunotherapy improves tumor responses in patients with early-stage neoplasms

4983- Dipy,  ATV,    Targeting tumor cell metabolism via the mevalonate pathway: Two hits are better than one
- Review, Var, NA
HMG-CoA↓, Statins are promising anticancer agents that target the mevalonate pathway
AntiTum↓, dipyridamole inhibits this feedback response and potentiates statin antitumor activity.
eff↑, this combination of 2 FDA-approved drugs has the potential to be fast-tracked to cancer patient care.

4685- EGCG,    Epigallocathechin gallate, polyphenol present in green tea, inhibits stem-like characteristics and epithelial-mesenchymal transition in nasopharyngeal cancer cell lines
- in-vitro, NPC, TW01 - in-vitro, NPC, TW06
CSCs↓, EGCG potently inhibited sphere formation and can eliminate the stem cell characteristics of NPC and inhibit the epithelial-mesenchymal transition (EMT) signatures.
EMT↓,
TumCMig↓, Inhibition on NPC sphere-derived cell colony formation, migration, and invasion by EGCG
TumCI↓,
OCT4↓, EGCG inhibited the expression of Klf-4 and Oct-4 in sphere-derived cells.
Snail↓, EGCG significantly inhibited the levels of Snail, Vimentin and increased E-Cadherin expression in a dose-dependent manner
Vim↓,
E-cadherin↓,
HSP70/HSPA5↓, EGCG suppresses the expression of HSP70 and HSP90, and exhibits anti-tumor activity in vitro and in vivo
HSP90↓,
AntiTum↓,

7645- IP6,  Ins,    Anticancer Properties of Inositol Hexaphosphate and Inositol: An Overview
AntiCan↑, A consistent and reproducible anticancer action of IP6 has been demonstrated in various experimental models.
TumCP↓, IP6 reduces cell proliferation, induces apoptosis and differentiation of malignant cells via PI3K, MAPK, PKC, AP-1 and NF-kappaB.
Apoptosis↑,
Diff↑,
p27/CDKN1B↓, down-regulates p27, inhibits pRB phosphorylation and cell cycle (23), reduces PI3K and consequently counteracts the activation of PKC/RAS/ERK pathway (23), downregulates Akt and ERK, leading to reduction of NF-kappaB and inhibition of inflammation.
pRB↓,
PI3K↓,
RAS↓,
ERK↓,
Akt↓,
NF-kB↓,
Inflam↓,
AntiTum↓, Studies demonstrated that continuous administration of 2% IP 6 in the drinking water, beginning 24 h after implantation of DU-145 prostate cancer cells, resulted in a 64% decrease in tumor burden

8095- KAE,    Kaempferol: A Key Emphasis to Its Anticancer Potential
- Review, Var, NA
*AntiBio↑, Kaempferol displays several pharmacological properties, among them antimicrobial, anti-inflammatory, antioxidant, antitumor, cardioprotective, neuroprotective, and antidiabetic activities, and is being applied in cancer chemotherapy.
*Inflam↓,
*AntiTum↓,
*antiOx↑, kaempferol contains hydroxyl groups at C3, C5, and C4, an oxo group at C4, and a double bond at C2-C3 that might explain its antioxidant activity
*cardioP↑,
*neuroP↑,
*AntiDiabetic↑,
Risk↓, Specifically, kaempferol-rich food has been linked to a decrease in the risk of developing some types of cancers, including skin, liver, and colon.
TumCCA↑, The mechanisms of action include apoptosis, cell cycle arrest at the G2/M phase, downregulation of epithelial-mesenchymal transition (EMT)-related markers, and phosphoinositide 3-kinase/protein kinase B signaling pathways.
EMT↓,
PI3K↓,
Akt↓, downregulation of signaling pathways and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT), expression of epithelial-mesenchymal transition (EMT)-related markers (N-cadherin, E-cadherin, Snail, and Slug), and matrix metallopeptidase 2 (MMP-2),
MMP2↓,
Casp3↑, Kaempferol also induces the activation of cysteine proteases involved in apoptosis initiation and execution, caspases-3, -7, -9, and Poly (ADP-ribose) polymerase (PARP)
Casp7↑,
Casp9↑,
PARP↑,
*ROS↓, therefore preventing the accumulation of reactive oxygen species (ROS) involved in cancer development
angioG↓, The inhibition of angiogenesis was also reported as well as the capacity of kaempferol to preserve normal cell viability
*BioAv↑, To overcome the low bioavailability of kaempferol, its combination with quercetin increase its bioavailability, consequently improving its bio-efficacy.
BioAv↑, nanoformulations (e.g., nanoparticles, nanoemulsions, nanoencapsulation) containing kaempferol will be extremely beneficial in improving their bioavailability and consequent efficacy and selectivity for mutated cells,
selectivity↑, while their effect on normal cells will be limited. kaempferol exerts protective effects in non-mutated cells, whereas it triggers apoptosis in those mutated ones.
GLUT1↓, kaempferol also lowers the glucose transporter 1 (GLUT1) mRNA levels and prevents the uptake of (3)H-deoxy-d-glucose ((3)H-DG) and monocarboxylate transporter 1 (MCT1)-
MCT1↓,
ROS↓, Blocked ROS generation, cell cycle arrest at G1 and G2/M arrest, and cell migration
ROS↑, This flavonoid also triggers ROS generation and apoptosis, through reduction of the thioredoxin concentrations, superoxide dismutase activity
Trx↓,
Cyt‑c↑, Kaempferol is also able to release cytochrome c via ROS generation triggering mitochondrial membrane potential loss and mitochondrial swelling and increasing the level of cleaved caspase-3
MMP↓,
miR-21↓, Kaempferol also decreases the expression level of miR-21, cytokine signaling 3 (SOCS3), signal transducer and activator of transcription 3 (STAT3), CDK1, cyclin B, PI3K/AKT/mTOR and p-mTOR signaling pathway, and hypoxia-inducible factor 1 (HIF-1) in
SOCS-3↓,
STAT3↓,
CDK1↓,
CycB/CCNB1↑,
HIF-1↓,
JAK1↑, enhanced the expression of Janus kinase 1 (JAK1), tyrosine kinase 2 (Tyk2), STAT1/2, endogenous interferon (IFN)-α-regulated genes, phosphatase and tensin homologue (PTEN)
PTEN↑,

8139- LF,    Androgen Receptor‐Induced Lactoferrin Accelerates Prostate Tumorigenesis Through Modulating Ferroptosis
- vitro+vivo, Pca, NA
Ferroptosis↓, Mechanistically, lactoferrin shields prostate cancer cells from iron‐induced ferroptosis by maintaining iron‐redox homeostasis.
AR↝, This work defines lactoferrin as: (i) an AR‐regulated ferroptosis suppressor,
Iron↝, (ii) a regulator of prostate cancer's “iron addiction,” and (iii) a candidate target for therapeutic exploitation of iron‐metabolic vulnerability.
Ferritin↑, This study demonstrates that transcription factor androgen receptor (AR) directly binds the LF promoter, driving lactoferrin overexpression to promote ferritin (FTH1/FTL) upregulation and inhibit p53‐ALOX12‐mediated ferroptosis in prostate cancer
P53↓,
eff↝, Lactoferrin Deficiency Delays Prostate Tumorigenesis in TRAMP Mice
other↝, The current study revealed that lactoferrin is a previously unrecognized oncogene in prostate cancer, elucidating a novel AR‐lactoferrin‐ferroptosis regulatory axis with potential therapeutic prospects.
AntiTum↓, Contrary to its established tumor‐suppressive functions, we find that in prostate cancer, lactoferrin can exhibit oncogenic properties, a function that is mechanistically linked to and dependent on AR signaling.


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↓, 1,   GSH↓, 1,   Iron↝, 1,   ROS↓, 1,   ROS↑, 5,   Trx↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

glucose↓, 1,   HMG-CoA↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Apoptosis↑, 4,   BAX↑, 2,   Bcl-2↓, 2,   Casp3↑, 2,   Casp7↑, 1,   Casp9↓, 1,   Casp9↑, 2,   Cyt‑c↑, 1,   Ferroptosis↓, 1,   iNOS↓, 1,   MCT1↓, 1,   p27/CDKN1B↓, 1,   p‑p38↑, 1,   TumCD↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↑, 1,   miR-21↓, 1,   other↝, 1,   PhotoS↑, 2,   pRB↓, 1,   sonoS↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,   HSP70/HSPA5↓, 1,   HSP90↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,   PARP↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CDK2↓, 1,   CycB/CCNB1↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CSCs↓, 1,   Diff↑, 1,   EMT↓, 2,   ERK↓, 1,   IGF-1↓, 1,   mTOR↓, 1,   OCT4↓, 1,   PI3K↓, 3,   PTEN↑, 1,   RAS↓, 1,   STAT3↓, 2,  

Migration(tgid=13) ⓘ

5LO↓, 1,   E-cadherin↓, 1,   Ki-67↓, 1,   MMP2↓, 1,   MMPs↓, 1,   Snail↓, 1,   TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 2,   Vim↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   HIF-1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL2↓, 1,   Imm↑, 1,   Inflam↓, 1,   JAK1↑, 1,   NF-kB↓, 2,   SOCS-3↓, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↝, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   ChemoSen↑, 1,   eff↓, 1,   eff↑, 6,   eff↝, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↝, 1,   Ferritin↑, 1,   Ki-67↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   AntiTum↓, 6,   cardioP↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   OS↑, 1,   Risk↓, 1,   toxicity↝, 1,  
Total Targets: 93

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   antiOx↑, 1,   ROS↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 1,   AntiTum↓, 2,   cardioP↑, 1,   neuroP↑, 1,   radioP↑, 1,  
Total Targets: 11

Scientific Paper Hit Count for: AntiTum, AntiTumor
1 Carnosic acid
1 Curcumin
1 diet FMD Fasting Mimicking Diet
1 Bortezomib
1 Dipyridamole
1 Atorvastatin
1 EGCG (Epigallocatechin Gallate)
1 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
1 Inositol
1 Kaempferol
1 Lactoferrin/Talactoferrin
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

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