CycD3 Cancer Research Results

CycD3, Cyclin D3: Click to Expand ⟱
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Cyclin D3 is a protein that plays a crucial role in the regulation of cell cycle progression.
Lineage-Specific Cell-Cycle Control
It is a member of the cyclin family of proteins, which are involved in the regulation of the cell cycle.
Cyclin D3 has been found to be overexpressed in various types of cancer, including breast, lung, colon, and prostate cancer.
Cyclin D3 has been shown to be involved in the regulation of cancer cell proliferation, and its overexpression has been linked to increased cell growth and survival.
Scientific Papers found: Click to Expand⟱
2639- Api,    Plant flavone apigenin: An emerging anticancer agent
- Review, Var, NA
*antiOx↑, Apigenin (4′, 5, 7-trihydroxyflavone), a major plant flavone, possessing antioxidant, anti-inflammatory, and anticancer properties
*Inflam↓,
AntiCan↑,
ChemoSen↑, Studies demonstrate that apigenin retain potent therapeutic properties alone and/or increases the efficacy of several chemotherapeutic drugs in combination on a variety of human cancers.
BioEnh↑, Apigenin’s anticancer effects could also be due to its differential effects in causing minimal toxicity to normal cells with delayed plasma clearance and slow decomposition in liver increasing the systemic bioavailability in pharmacokinetic studies.
chemoPv↑, apigenin highlighting its potential activity as a chemopreventive and therapeutic agent.
IL6↓, In taxol-resistant ovarian cancer cells, apigenin caused down regulation of TAM family of tyrosine kinase receptors and also caused inhibition of IL-6/STAT3 axis, thereby attenuating proliferation.
STAT3↓,
NF-kB↓, apigenin treatment effectively inhibited NF-κB activation, scavenged free radicals, and stimulated MUC-2 secretion
IL8↓, interleukin (IL)-6, and IL-8
eff↝, The anti-proliferative effects of apigenin was significantly higher in breast cancer cells over-expressing HER2/neu but was much less efficacious in restricting the growth of cell lines expressing HER2/neu at basal levels
Akt↓, Apigenin interferes in the cell survival pathway by inhibiting Akt function by directly blocking PI3K activity
PI3K↓,
HER2/EBBR2↓, apigenin administration led to the depletion of HER2/neu protein in vivo
cycD1/CCND1↓, Apigenin treatment in breast cancer cells also results in decreased expression of cyclin D1, D3, and cdk4 and increased quantities of p27 protein
CycD3↓,
p27↑,
FOXO3↑, In triple-negative breast cancer cells, apigenin induces apoptosis by inhibiting the PI3K/Akt pathway thereby increasing FOXO3a expression
STAT3↓, In addition, apigenin also down-regulated STAT3 target genes MMP-2, MMP-9, VEGF and Twist1, which are involved in cell migration and invasion of breast cancer cells [
MMP2↓,
MMP9↓,
VEGF↓, Apigenin acts on the HIF-1 binding site, which decreases HIF-1α, but not the HIF-1β subunit, thereby inhibiting VEGF.
Twist↓,
MMP↓, Apigenin treatment of HGC-27 and SGC-7901 gastric cancer cells resulted in the inhibition of proliferation followed by mitochondrial depolarization resulting in apoptosis
ROS↑, Further studies revealed apigenin-induced apoptosis in hepatoma tumor cells by utilizing ROS generated through the activation of the NADPH oxidase
NADPH↑,
NRF2↓, Apigenin significantly sensitized doxorubicin-resistant BEL-7402 (BEL-7402/ADM) cells to doxorubicin (ADM) and increased the intracellular concentration of ADM by reducing Nrf2-
SOD↓, In human cervical epithelial carcinoma HeLa cells combination of apigenin and paclitaxel significantly increased inhibition of cell proliferation, suppressing the activity of SOD, inducing ROS accumulation leading to apoptosis by activation of caspas
COX2↓, melanoma skin cancer model where apigenin inhibited COX-2 that promotes proliferation and tumorigenesis
p38↑, Additionally, it was shown that apigenin treatment in a late phase involves the activation of p38 and PKCδ to modulate Hsp27, thus leading to apoptosis
Telomerase↓, apigenin inhibits cell growth and diminishes telomerase activity in human-derived leukemia cells
HDAC↓, demonstrated the role of apigenin as a histone deacetylase inhibitor. As such, apigenin acts on HDAC1 and HDAC3
HDAC1↓,
HDAC3↓,
Hif1a↓, Apigenin acts on the HIF-1 binding site, which decreases HIF-1α, but not the HIF-1β subunit, thereby inhibiting VEGF.
angioG↓, Moreover, apigenin was found to inhibit angiogenesis, as suggested by decreased HIF-1α and VEGF expression in cancer cells
uPA↓, Furthermore, apigenin intake resulted in marked inhibition of p-Akt, p-ERK1/2, VEGF, uPA, MMP-2 and MMP-9, corresponding with tumor growth and metastasis inhibition in TRAMP mice
Ca+2↑, Neuroblastoma SH-SY5Y cells treated with apigenin led to induction of apoptosis, accompanied by higher levels of intracellular free [Ca(2+)] and shift in Bax:Bcl-2 ratio in favor of apoptosis, cytochrome c release, followed by activation casp-9, 12
Bax:Bcl2↑,
Cyt‑c↑,
Casp9↑,
Casp12↑,
Casp3↑, Apigenin also augmented caspase-3 activity and PARP cleavage
cl‑PARP↑,
E-cadherin↑, Apigenin treatment resulted in higher levels of E-cadherin and reduced levels of nuclear β-catenin, c-Myc, and cyclin D1 in the prostates of TRAMP mice.
β-catenin/ZEB1↓,
cMyc↓,
CDK4↓, apigenin exposure led to decreased levels of cell cycle regulatory proteins including cyclin D1, D2 and E and their regulatory partners CDK2, 4, and 6
CDK2↓,
CDK6↓,
IGF-1↓, A reduction in the IGF-1 and increase in IGFBP-3 levels in the serum and the dorsolateral prostate was observed in apigenin-treated mice.
CK2↓, benefits of apigenin as a CK2 inhibitor in the treatment of human cervical cancer by targeting cancer stem cells
CSCs↓,
FAK↓, Apigenin inhibited the tobacco-derived carcinogen-mediated cell proliferation and migration involving the β-AR and its downstream signals FAK and ERK activation
Gli↓, Apigenin inhibited the self-renewal capacity of SKOV3 sphere-forming cells (SFC) by downregulating Gli1 regulated by CK2α
GLUT1↓, Apigenin induces apoptosis and slows cell growth through metabolic and oxidative stress as a consequence of the down-regulation of glucose transporter 1 (GLUT1).

5639- BCA,    Biochanin A Induces Apoptosis in MCF-7 Breast Cancer Cells through Mitochondrial Pathway and Pi3K/AKT Inhibition
- in-vitro, BC, NA
TumCP↓, Biochanin A inhibited cell proliferation, increased reactive oxygen species formation, and induced apoptosis.
ROS↑,
Apoptosis↑,
Bcl-2↓, Biochanin A-treated cells exhibited lower expression of the Bcl-2, p-PI3K and p-AKT and higher expression of proapoptotic genes, including Bax, Caspase-3, Caspase-9, and cytochrome c.
p‑PI3K↓,
p‑Akt↓,
BAX↑,
Casp3↑,
Casp9↑,
Cyt‑c↑,
CycD3↓, gene expression levels of cyclin D3, cyclin B1, CDK1, CDK2, and CDK4 were downregulated
CycB/CCNB1↓,
CDK1↓,
CDK2↓,
CDK4↓,
P21↑, while the expression levels of p21, p27, and p53 were significantly upregulated
p27↑,
P53↑,
tumCV↓, These results suggest that Biochanin A can suppress the viability of breast cancer cells and induce apoptosis via the mitochondrial pathway
PI3K↓, inhibition of the Pi3K/Akt signaling pathway and modulation of cell cycle markers.
Akt↓,

5866- CA,    Carnosic acid inhibits STAT3 signaling and induces apoptosis through generation of ROS in human colon cancer HCT116 cells
- in-vitro, CRC, HCT116 - in-vitro, Colon, SW480 - in-vitro, Colon, HT29
tumCV↓, CA treatment significantly reduced the viability of human colon cancer HCT116, SW480, and HT-29 cells.
Apoptosis↑, Treatment with CA induced apoptosis, which was associated with the induction of p53 and Bax, inhibition of Mdm2, Bcl-2, and Bcl-xl expression, activation of caspase-9, and -3, and the cleavage of PARP in HCT116 cells.
P53↑,
BAX↑,
MDM2↓,
Bcl-2↓,
Bcl-xL↓,
Casp9↑,
Casp3↑,
cl‑PARP↑,
STAT3↓, CA inhibited the constitutive phosphorylation, the DNA binding and the reporter gene activity of STAT3
survivin↓, CA attenuated the expression of STAT3 target gene products, such as survivin, cyclin D1, D2, and D3
cycD1/CCND1↓,
CycD3↓,
ROS↑, CA treatment induced the generation of ROS in these colon cancer cells.
eff↓, Pretreatment of cells with ROS scavenger N-acetyl cysteine abrogated the inhibitory effect of CA on the JAK2-STAT3/Src-STAT3 signaling and rescued cells from CA-induced apoptosis
eff↑, However, L-buthionine-sulfoximine, a pharmacological inhibitor of GSH synthesis, increased CA-induced ROS production, thereby potentiating apoptotic effect of CA.

803- GAR,    Induction of p21(Waf1/Cip1) by garcinol via downregulation of p38-MAPK signaling in p53-independent H1299 lung cancer
- in-vitro, Lung, H1299 - in-vitro, Lung, H460
TumCP↓,
TumCCA↑, G1 cell cycle arrest (H1299)
CDK2↓,
CDK4↓,
cycD1/CCND1↓,
CycD3↓,
cycE/CCNE↑, cyclin E and cyclin-dependent kinase 6 (CDK6) were increased in garcinol-treated H1299 cells
CDK6↑,
P21↑,
p27↑,
ERK↓,
MAPK↓,

4791- Lyco,    Investigating into anti-cancer potential of lycopene: Molecular targets
- Review, Var, NA
*antiOx↑, Lycopene, the main pigment of tomatoes, possess the strongest antioxidant activity among carotenoids. Lycopene has unique structure and chemical properties.
TumCP↓, the anticancer of lycopene is also considered to be an important determinant of tumor development including the inhibition of cell proliferation, inhibition of cell cycle progression, induction of apoptosis, inhibition of cell invasion, angiogenesis
TumCCA↓,
Apoptosis↑,
TumCI↓,
angioG↓,
TumMeta↓,
*Risk↓, and may be associated with a decreased risk of different types of cancer.
cycD1/CCND1↓, Several studies suggested lycopene decreased cell cycle related proteins, such as cyclin D1, D3 and E, the cyclin-dependent kinases 2 and 4, bcl-2, while decreased phospho-Akt levels and increased p21, p27, p53 and bax levels and in Bax: Bcl-2 ratio
CycD3↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
Bcl-2↓,
P21↑,
p27↑,
P53↑,
BAX↑,
selectivity↑, lycopene selectively inhibited cell growth in MCF-7 human breast cancer cells but not in the MCF-10 mammary epithelial cells
MMP↓, When treating LNCaP human prostate cancer cells with lycopene, the decreased mitochondrial function could be observed.
Cyt‑c↑, release of mitochondrial cytochrome c and finally led to apoptosis
Wnt↓, Lycopene could inhibit Wnt-TCF signaling pathway in cancer cells.
eff↑, Lycopene could synergistically increase QC anticancer activity and inhibit Wnt-TCF signaling in cancer cells.
PPARγ↑, Lycopene could inhibit the growth of cancer cells by activating the PPARγ – LXRα - ABCA1 pathway and decreasing cellular total cholesterol levels
LDL↓,
Akt↓, Lycopene suppressed Akt activation and non-phosphorylated β-Catenin,
PI3K↓, inhibited the proliferation of colon cancer HT-29 cells, which was associated with suppressing PI3K/Akt/mTOR signaling pathway
mTOR↓,
PDGF↓, Lycopene, however, could inhibit PDGF-BB-induced signaling and cell migration in both human cultured skin fibroblasts and melanoma-derived fibroblasts
NF-kB↓, anticancer properties of lycopene may occur to play its role through the inhibition of the NF-κB signaling pathway
eff↑, lycopene increased the sensitization of cervical cancer cells to cisplatin via the suppression of NF-κB-mediated inflammatory responses, and the modulation of Nrf2-mediated oxidative stress


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

NRF2↓, 1,   ROS↑, 3,   SOD↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,   LDL↓, 1,   NADPH↑, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 3,   p‑Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Bcl-xL↓, 1,   Casp12↑, 1,   Casp3↑, 3,   Casp9↑, 3,   CK2↓, 1,   Cyt‑c↑, 3,   MAPK↓, 1,   MDM2↓, 1,   p27↑, 4,   p38↑, 1,   survivin↓, 1,   Telomerase↓, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 2,  

DNA Damage & Repair ⓘ

P53↑, 3,   cl‑PARP↑, 2,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 4,   CDK4↓, 4,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 4,   CycD3↓, 5,   cycE/CCNE↓, 1,   cycE/CCNE↑, 1,   P21↑, 3,   TumCCA↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   ERK↓, 1,   FOXO3↑, 1,   Gli↓, 1,   HDAC↓, 1,   HDAC1↓, 1,   HDAC3↓, 1,   IGF-1↓, 1,   mTOR↓, 1,   PI3K↓, 3,   p‑PI3K↓, 1,   STAT3↓, 3,   Wnt↓, 1,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↑, 1,   FAK↓, 1,   MMP2↓, 1,   MMP9↓, 1,   PDGF↓, 1,   TumCI↓, 1,   TumCP↓, 3,   TumMeta↓, 1,   Twist↓, 1,   uPA↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   Hif1a↓, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   IL8↓, 1,   NF-kB↓, 2,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,   CDK6↑, 1,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 1,   ChemoSen↑, 1,   eff↓, 1,   eff↑, 3,   eff↝, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

HER2/EBBR2↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   chemoPv↑, 1,  
Total Targets: 86

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

Risk↓, 1,  
Total Targets: 3

Scientific Paper Hit Count for: CycD3, Cyclin D3
1 Apigenin (mainly Parsley)
1 Biochanin A
1 Carnosic acid
1 Garcinol
1 Lycopene
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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