cycD1/CCND1 Cancer Research Results

cycD1/CCND1, cyclin D1 pathway: Click to Expand ⟱
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Type:
Also called CCND1 Gatekeeper of Cell-Cycle Commitment
The main function of cyclin D1 is to maintain cell cycle and to promote cell proliferation. Cyclin D1 is a key regulatory protein involved in the cell cycle, particularly in the transition from the G1 phase to the S phase. It is part of the cyclin-dependent kinase (CDK) complex, where it binds to CDK4 or CDK6 to promote cell cycle progression.
Cyclin D1 is crucial for the regulation of the cell cycle. Overexpression or dysregulation of cyclin D1 can lead to uncontrolled cell proliferation, a hallmark of cancer.
Cyclin D1 is often found to be overexpressed in various cancers.
Cyclin D1 can interact with tumor suppressor proteins, such as retinoblastoma (Rb). When cyclin D1 is overexpressed, it can lead to the phosphorylation and inactivation of Rb, releasing E2F transcription factors that promote the expression of genes required for DNA synthesis and cell cycle progression.
Cyclin D1 is influenced by various signaling pathways, including the PI3K/Akt and MAPK pathways, which are often activated in cancer.
In some cancers, high levels of cyclin D1 expression have been associated with poor prognosis, making it a potential biomarker for cancer progression and treatment response.
Scientific Papers found: Click to Expand⟱
2733- BetA,    Betulinic Acid Inhibits Cell Proliferation in Human Oral Squamous Cell Carcinoma via Modulating ROS-Regulated p53 Signaling
- in-vitro, Oral, KB - in-vivo, NA, NA
TumCP↓, BA dose-dependently inhibited KB cell proliferation and decreased implanted tumor volume.
TumVol↓,
mt-Apoptosis↑, BA significantly promoted mitochondrial apoptosis, as reflected by an increase in TUNEL+ cells and the activities of caspases 3 and 9, an increase in Bax expression, and a decrease in Bcl-2 expression and the mitochondrial oxygen consumption rate.
Casp3↑,
Casp9↑,
BAX↑,
Bcl-2↑,
OCR↓, BA dose-dependently decreased the oxygen consumption rate, indicating that BA induced a significant mitochondrial dysfunction
TumCCA↑, BA significantly increased cell population in the G0/G1 phase and decreases the S phase cell number, indicating the occurrence of G0/G1 cell cycle arrest.
ROS↑, ROS generation was significantly increased by BA
eff↓, and antioxidant NAC treatment markedly inhibited the effect of BA on apoptosis, cell cycle arrest, and proliferation.
P53↑, BA dose-dependently increased p53 expression in KB cells and implanted tumors.
STAT3↓, Inhibition of STAT3 Signaling Is Involved in BA-Induced Suppression of Cell Proliferation
cycD1/CCND1↑, We found that BA mainly increased the mRNA expression of cyclin D1 but had no significant effect on cyclin E, CDK2, CDK4, or CDK6 expression.

7284- Gins,  5-FU,    Ginsenoside Rg3 enhances the anticancer effect of 5-FU in colon cancer cells via the PI3K/AKT pathway
- vitro+vivo, CRC, SW-620 - in-vitro, CRC, LoVo
ChemoSen↑, The results revealed that combined treatment of Rg3 and 5-FU significantly enhanced the inhibition of the proliferation, colony formation, invasion and migration of human colon cancer cells (SW620 and LOVO) in vitro.
TumCP↓,
TumCI↓,
TumCMig↓,
APAF1↑, Rg3 and 5-FU significantly enhanced the apoptosis of colon cancer cells by activating the Apaf1/caspase 9/caspase 3 pathway and arrested the cell cycle of the colon cancer cells in G0/G1
Casp9↑,
Casp3↑,
TumCCA↑,
cycD1/CCND1↑, by promoting the expression of Cyclin D1, CDK2 and CDK4.
CDK2↑,
CDK4↑,
PI3K↓, PI3K/AKT signaling pathway in colon cancer cells was suppressed by Rg3 and 5-FU.
Akt↓,

7781- ISL,    Perspectives on the Role of Isoliquiritigenin in Cancer
- Review, Var, NA
*BioAv↝, through different routes of administrations, including intravenously (IV), via hypodermic (IH) or intraperitoneal (IP) injection, and orally, have indicated that ISL exhibits a robust absorption capacity (absorption rate: ~60–90 min; oral absorptio
*BBB↓, ISL distribution mainly relies on the blood circulation, with the brain showing the lowest level of ISL due to the blood–brain barrier (BBB)
*BioAv↑, To improve solubility, enhancing its bioavailability and distribution, encapsulated ISL nanoparticles or nano-ISL have been developed.
selectivity↑, A selective cytotoxicity effect of ISL has been reported (Table 2 and Table 3), and the effective dose in tumor cell lines shows very little cytotoxic effect on normal cells.
*neuroP↑, Figure 4
*Inflam↓,
NF-kB↓,
TNF-α↓,
IL6↓,
IL1β↓,
IL10↓,
ICAM-1↓,
COX2/PTGS2↓,
PPARγ↑,
MMP2↓,
cFos↓,
VEGF↓,
CHOP/DDIT3↓,
CTSK↓,
CycB/CCNB1↑,
cycD1/CCND1↑,
TOP2↑,
PI3K↓, ISL also can inhibit the PI3K/AKT pathway and thus suppresses EMT and increases the antiproliferative effect
Akt↓,
mTOR↓,
MMP9↓,
TIMP1↓,
ChemoSen↑, ISL not only inhibits cancer cell growth by inducing apoptosis and autophagy, but can also enhance chemosensitivity
CSCs↓, ISL can interact synergistically with these first-line chemotherapy drugs through mediating cell death (apoptosis) and autophagy and suppressing breast CSCs

8237- LCA,    Role of Licochalcone A in Potential Pharmacological Therapy: A Review
- Review, Var, NA
*other↝, Licorice always functions as an adjuvant drug in traditional Chinese medicine to reduce the toxicity of other medicinal herbs or enhance their pharmacological effects.
*Inflam↓, LA demonstrates various pharmacological properties, including anti-inflammation, antibacterial, antioxidant, anti-parasitic, bone protection, neuroprotection, skin protection, and blood glucose and lipid regulation.
*Bacteria↓,
*antiOx↑,
*AntiP↑,
*neuroP↑,
*glucose↝,
*lipid-P↓,
PKCδ↓, Downregulation of PKCε, p70S6K, and Akt is also described
P70S6K↓,
Akt↓,
ER Stress↑, LA induced ER stress in HepG2 cells to induce apoptosis
Apoptosis↑,
Ca+2↑, enhancing cytosolic Ca2+ release from the ER
PI3K↓, apoptosis of MCF-7 by inhibiting PI3K-Akt-mTOR signaling, thereby increasing caspase-3 activity, decreasing expression of B-cell lymphoma-2, and triggering the release of cytochrome from mitochondria into the cytoplasm
mTOR↓,
Casp3↑,
Bcl-2↓,
Cyt‑c↑,
BAX↑, upregulation of Bax expression and PARP cleavage, downregulation of Bcl-2 and Cyclin D1, and accumulation of reactive oxygen species (ROS)
cl‑PARP↑,
cycD1/CCND1↑,
ROS↑,
CHOP/DDIT3↑, CHOP expression was elevated in parallel
ERK↑, LA significantly activated ERK and p38 in A549 and H460 cells in a time-dependent manner.
p38↑,
JNK↓, LA also inhibited the activity of JNK, suppressed the expression of c-IAP1, c-IAP2, XIAP, Survivin, c-FLIPL, and RIP1, and attenuated LA-induced induction of autophagy
IAP1↓,
XIAP↓,
survivin↓,
cFLIP↓,
RIP1↓,
EGFR↓, promoted the degradation of EGFR, Met, Her2
MET↓,
HER2/EBBR2↓,
p‑4E-BP1↓, LA may inhibit the phosphorylation of 4EBP1 (Ser 65) and activate the PERK-eIF2α pathway to inhibit PD-L1 translation
PERK↑,
eIF2α↑,
PD-L1↓,
HK2↓, Hexokinase 2Â (HK2) expression was downregulated at a lower dose, attenuating glycolysis elevation and inducing apoptosis in MKN-45 and SGC7901 cells
Glycolysis↓,
Sp1/3/4↓, LA induced apoptosis via downregulating the expression of specificity protein 1 (Sp1), upregulating Bax, Bid, Bcl-xl, caspase-3, and PARP cleavage with doses of 10–40 μM
FasL↑, LA induced apoptosis in KB cells, relying on activation of caspase-dependent factor associated suicide ligand (FasL) mediated death receptor pathway.
MMP↓, reducing mitochondrial membrane potential and inhibiting ATP production in vitro
ATP↓,
TumAuto↑, The literature also showed that LA induced apoptosis and autophagy in SiHa
WEE1↑, LA blocked the cell cycle in HepG2 cells by increasing the expression of Weel, P21, Cyclin D1, and JNK1 and decreasing the expression of Survivin, Cyclin B1, and CDK1 using doses of 30–70 μM
P21↑,
CDK1↓,
TumCCA↑,
TumCMig↓, LA exhibited the ability to inhibit migration and invasion of A549 and H460 cells at relatively lower doses (2–20 μM)
TumCI↓,
ABCG2↓, downregulating the expression of breast cancer resistance protein (BCRP)
HSP90↓, LA also reduced Hsp90 activity in gefitinib-resistant NSCLC cells (H1975) via binding to the N-terminal ATP binding site of Hsp90 to reduce drug resistance
T-Cell↑, LA (40 mg/kg) to C3H/HeN mice bearing UM-UC-3 cells enhanced the activity of cytotoxic T lymphocytes and counts of CD4+ CD25+ Foxp3+ T regulatory T cells. Thus, LA might treat bladder cancer by modulating the tumor immune microenvironment
CD4+↑,
CD25+↑,
FOXP3↑,
Imm↝,
*Inflam↓, LA demonstrates anti-inflammatory activity via interaction with MAPK, NF-κB, NLRP3, and Nrf2 signaling in the acute lung, kidney, and liver injury (acute inflammation) and arthritis and asthma
*NF-kB↓,
*NRF2↑,
*AntiArt↑,

8244- LCA,    Licochalcone A from licorice root, an inhibitor of human hepatoma cell growth via induction of cell apoptosis and cell cycle arrest
- in-vitro, Liver, HepG2
TumCP↓, LCA inhibited the proliferation of HepG2 cells with IC50 (65.96 μM) for 24 h and IC50 (44.13 μM) for 48 h and caused significant morphological changes and also led to intracellular ROS generation.
ROS↑,
TumCCA↑, LCA affected HepG2 cell growth by terminating cell cycle development at G2/M transition and further induced the apoptosis process.
Apoptosis↑,
survivin↓, The mRNA expression of genes involved in cell cycles such as Survivin, Cyclin B1, and CDK1 were reduced
CycB/CCNB1↓,
CDK1↓,
WEE1↑, while, Weel, P21, Cyclin D1, and JNK1 showed increased mRNA expression.
P21↑,
cycD1/CCND1↑,
JNK↑,
TNFRSF25/DR3/APO3/LARD/TRAMP/WSL1↑, The anti-cancer action involved increased mRNA expression of DR3, DR5, caspases-3, caspases-8, caspases-10, Fas, Bad, Bax, Bcl-2, Bak, and PUMA
DR5↑,
Casp3↑,
Casp8↑,
Casp10↑,
Fas↑,
BAD↑,
BAX↑,
PUMA↑,
PKCδ↓, besides, decreased level of PKCε, p70S6K, and Akt.
P70S6K↓,
Akt↓,

993- RES,    Resveratrol reverses the Warburg effect by targeting the pyruvate dehydrogenase complex in colon cancer cells
- in-vitro, CRC, Caco-2 - in-vivo, Nor, HCEC 1CT
TumCG↓,
Glycolysis↓,
PPP↓,
ATP↑, significant increase (20%) in ATP production
PDH↑, Resveratrol targets the pyruvate dehydrogenase (PDH) complex, a key mitochondrial gatekeeper of energy metabolism, leading to an enhanced PDH activity.
Ca+2↝, resveratrol is a potent modulator of many cellular Ca2+ signaling pathways. Ca2+ is a key mediator of the effect of resveratrol on the oxidative capacity of colon cancer cells.
TumCP↓,
lactateProd↓,
OCR↑, increase of oxygen consumption rate (OCR) both in normal colonic epithelial HCEC 1CT cells
ECAR↓, Following treatment with resveratrol (10 µM, 48 hr), the ECAR was unchanged in normal HCEC 1CT cells, whereas it was significantly reduced (31%) in HCEC 1CT RPA cells ****
*ECAR∅, Following treatment with resveratrol (10 µM, 48 hr), the ECAR was unchanged in normal HCEC 1CT cells
*other?, Resveratrol promotes a shift from respiration to glycolysis in cancer-like cells, but not in normal colonocytes
cycE/CCNE↑, Resveratrol inhibited cell cycle progression by enhancing the levels of cyclin E and cyclin A
cycA1/CCNA1↑,
TumCCA↑,
cycD1/CCND1↑, and by decreasing cyclin D1
OXPHOS↑, Taken together, these observations indicate that exposure to resveratrol leads to a metabolic reorientation from aerobic glycolysis toward OXPHOS.

1730- SFN,    Sulforaphane: An emergent anti-cancer stem cell agent
- Review, Var, NA
BioAv↓, When exposed to high temperatures during meal preparation, myrosinase can be degraded, lose its function, and subsequently compromise the synthesis of SFN.
BioAv↑, eating raw cruciferous vegetables, instead of heating them can significantly improve the biodisponibility of SFN and its subsequent beneficial effects.
GSTA1↑, induction of Phase II enzymes [glutathione S-transferase (GST)
P450↓, (cytochrome P450, CYP) inhibition
TumCCA↑, herb-derived agent can also promote cell cycle arrest and apoptosis by regulating different signaling pathways including Nuclear Factor erythroid Related Factor 2 (Nrf2)-Keap1 and NF-κB.
HDAC↓, modulate the activity of some epigenetic factors, such as histone deacetylases (HDAC),
P21↑, upregulation of p21 and p27,
p27/CDKN1B↑,
DNMT1↓, SFN was able to decrease the expression of DNMT1 and DNMT3 in LnCap prostate cancer cells
DNMT3A↓,
cycD1/CCND1↑, reduce methylation in Cyclin D2 promoter, thus inducing Cyclin D2 gene expression in those cells
DNAdam↑, SFN induced DNA damage, enhanced Bax expression and the release of cytochrome C followed by apoptosis
BAX↑,
Cyt‑c↑,
Apoptosis↑,
ROS↑, SFN increased reactive oxygen species (ROS), apoptosis-inducing factor (AIF)
AIF↑,
CDK1↑,
Casp3↑, activation of caspase-3, -8, and -9
Casp8↑,
Casp9↑,
NRF2↑, SFN significantly activated the major antioxidant marker Nrf2 and decreased NFκB, TNF-α, IL-1β
NF-kB↓,
TNF-α↓,
IL1β↓,
CSCs↓, SFN, have attracted attention due to their anti-CSC effect
CD133↓,
CD44↓,
ALDH↓,
Nanog↓,
OCT4↓,
hTERT/TERT↓,
MMP2↓,
EMT↓, SFN was reported to inhibit EMT and metastasis in the NSCLC, the cell lines H1299
ALDH1A1↓, ALDH1A1), Wnt3, and Notch4, other CSC-related genes inhibited by SFN treatment
Wnt↓,
NOTCH↓, SFN can inhibit aberrantly activated embryonic pathways in CSCs, including Sonic Hedgehog (SHH), Wnt/β-catenin, Cripto-1 (CR-1), and Notch.
ChemoSen↑, These results suggest that the antioxidant properties of SFN do not impact the cytotoxicity of antineoplastic drugs, but on the contrary, seems to improve it.
*Ki-67↓, Ki-67 and HDAC3 levels significantly decreased in benign breast tissues, and there was also a reduction in HDAC activity in blood cells
*HDAC3↓,
*HDAC↓,

1733- SFN,    Sonic Hedgehog Signaling Inhibition Provides Opportunities for Targeted Therapy by Sulforaphane in Regulating Pancreatic Cancer Stem Cell Self-Renewal
- in-vitro, PC, PanCSC - in-vitro, Nor, HPNE - in-vitro, Nor, HNPSC
CSCs↓, In an in vitro model, human pancreatic CSCs derived spheres were significantly inhibited on treatment with SFN
Shh↓, SFN inhibited the components of Shh pathway and Gli transcriptional activity
Gli↓,
Nanog↓, suppressing the expression of pluripotency maintaining factors (Nanog and Oct-4) as well as PDGFRα and Cyclin D1
OCT4↓,
PDGFRA↓,
cycD1/CCND1↑,
Apoptosis↑, SFN induced apoptosis by inhibition of BCL-2 and activation of caspases
Casp↑,
Smo↓, SFN inhibited the expression of Smo, Gli1 and Gli2.
Gli1↓,
GLI2↓,
Bcl-2↓, SFN induced apoptosis in pancreatic CSCs by inhibiting Bcl-2 expression and through the activation of caspase 3/7
Casp3↑,
Casp7↑,


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:


NA, unassigned(tgid=0) ⓘ

CTSK↓, 1,   TNFRSF25/DR3/APO3/LARD/TRAMP/WSL1↑, 1,   WEE1↑, 2,  

Redox & Oxidative Stress(tgid=1) ⓘ

GSTA1↑, 1,   NRF2↑, 1,   OXPHOS↑, 1,   ROS↑, 4,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   ATP↓, 1,   ATP↑, 1,   MMP↓, 1,   OCR↓, 1,   OCR↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ECAR↓, 1,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 1,   PDH↑, 1,   PPARγ↑, 1,   PPP↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 4,   APAF1↑, 1,   Apoptosis↑, 4,   mt-Apoptosis↑, 1,   BAD↑, 1,   BAX↑, 4,   Bcl-2↓, 2,   Bcl-2↑, 1,   Casp↑, 1,   Casp10↑, 1,   Casp3↑, 6,   Casp7↑, 1,   Casp8↑, 2,   Casp9↑, 3,   cFLIP↓, 1,   Cyt‑c↑, 2,   DR5↑, 1,   Fas↑, 1,   FasL↑, 1,   hTERT/TERT↓, 1,   IAP1↓, 1,   JNK↓, 1,   JNK↑, 1,   p27/CDKN1B↑, 1,   p38↑, 1,   PUMA↑, 1,   RIP1↓, 1,   survivin↓, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,   Sp1/3/4↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   CHOP/DDIT3↑, 1,   eIF2α↑, 1,   ER Stress↑, 1,   HSP90↓, 1,   PERK↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   DNMT1↓, 1,   DNMT3A↓, 1,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 2,   CDK1↑, 1,   CDK2↑, 1,   CDK4↑, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↑, 8,   cycE/CCNE↑, 1,   P21↑, 3,   TumCCA↑, 6,  

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

p‑4E-BP1↓, 1,   ALDH↓, 1,   ALDH1A1↓, 1,   CD133↓, 1,   CD44↓, 1,   cFos↓, 1,   CSCs↓, 3,   EMT↓, 1,   ERK↑, 1,   Gli↓, 1,   Gli1↓, 1,   HDAC↓, 1,   mTOR↓, 2,   Nanog↓, 2,   NOTCH↓, 1,   OCT4↓, 2,   P70S6K↓, 2,   PDGFRA↓, 1,   PI3K↓, 3,   Shh↓, 1,   Smo↓, 1,   STAT3↓, 1,   TOP2↑, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   Ca+2↝, 1,   GLI2↓, 1,   MET↓, 1,   MMP2↓, 2,   MMP9↓, 1,   PKCδ↓, 2,   TIMP1↓, 1,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 4,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD25+↑, 1,   CD4+↑, 1,   COX2/PTGS2↓, 1,   FOXP3↑, 1,   ICAM-1↓, 1,   IL10↓, 1,   IL1β↓, 2,   IL6↓, 1,   Imm↝, 1,   NF-kB↓, 2,   PD-L1↓, 1,   T-Cell↑, 1,   TNF-α↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABCG2↓, 1,   BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 3,   eff↓, 1,   P450↓, 1,   selectivity↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   HER2/EBBR2↓, 1,   hTERT/TERT↓, 1,   IL6↓, 1,   PD-L1↓, 1,  

Functional Outcomes(tgid=23) ⓘ

TumVol↓, 1,  
Total Targets: 138

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1,   AntiP↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   lipid-P↓, 1,   NRF2↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ECAR∅, 1,   glucose↝, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other?, 1,   other↝, 1,  

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

HDAC↓, 1,   HDAC3↓, 1,  

Migration(tgid=13) ⓘ

Ki-67↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 3,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   BioAv↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Ki-67↓, 1,  

Functional Outcomes(tgid=23) ⓘ

neuroP↑, 2,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 20

Scientific Paper Hit Count for: cycD1/CCND1, cyclin D1 pathway
2 Licochalcone A
2 Sulforaphane (mainly Broccoli)
1 Betulinic acid
1 Ginseng
1 5-fluorouracil
1 Isoliquiritigenin
1 Resveratrol
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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