cycE/CCNE Cancer Research Results
cycE/CCNE, Cyclin E: Click to Expand ⟱
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Cyclin E regulates multiple downstream molecules, such as the retinoblastoma susceptibility gene (RB1) and the transcription factor E2F.
Cyclin E (Cyclin E1 and Cyclin E2) is the key regulator of the late G1 → S-phase transition.
Cyclin E is a prognostic marker in breast cancer, its altered expression increased with the increasing stage and grade of the tumor.
Cyclin E is a regulatory protein that plays a critical role in the cell cycle, particularly in the transition from the G1 phase to the S phase. Its expression levels can significantly influence cancer progression and patient prognosis.
Cyclin E expression is frequently elevated in various cancers and is generally associated with poor prognosis. Its role in promoting cell cycle progression makes it a potential biomarker for tumor aggressiveness and patient outcomes.
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Scientific Papers found: Click to Expand⟱
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Review, |
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in-vitro, |
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BV2 |
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ROS⇅, Like other flavonoids, baicalein can be either anti-oxidant or pro-oxidant, depending on its metabolism and concentration.
ROS↑, It is reported that baicalein generated ROS, subsequently caused endoplasmic reticulum (ER) stress, activated Ca2+-dependent mitochondrial death pathway, finally triggered apoptosis
ER Stress↑,
Ca+2↑,
Apoptosis↑,
eff↑, Due to this, ROS production is a mechanism shared by all non-surgical therapeutic approaches for cancer, including chemotherapy, radiotherapy and photodynamic therapy
DR5↑, baicalein-induced ROS generation up-regulated DR5 expression and then activated the extrinsic apoptotic pathway in human prostate cancer cells
12LOX↓, Baicalein is known as a 12-LOX inhibitor.
Cyt‑c↑, It markedly induced the release of Cytochrome c from mitochondria into the cytosol and activated Caspase-9, Caspase-7, and Caspase-3, concomitant with cleavage of the Caspase-3 substrate poly(ADP-ribose) polymerase
Casp7↑,
Casp9↑,
Casp3↑,
cl‑PARP↑,
TumCCA↑, Baicalein induces G1/S arrest due to increased Cyclin E expression, a major factor in the regulation of the G1/S checkpoint of the cell cycle, accompanied by reduced levels of Cdk 4 and Cyclin D1 in human lung squamous carcinoma (CH27) cells
cycE/CCNE↑,
CDK4↓,
cycD1/CCND1↓,
VEGF↓, In ovarian cancer cells, baicalein effectively lowered the protein level of VEGF, c-Myc, HIF-α, and NFκB
cMyc↓,
Hif1a↓,
NF-kB↓,
BioEnh↑, curcumin and high-dose (−)-epicatechin were demonstrated to subsequently increase the absorption of baicalein
BioEnh↑, Baicalein can increase the oral bioavailability of tamoxifen by inhibiting cytochrome P450 (CYP) 3A4-mediated metabolism of tamoxifen in the small intestine and/or liver,
P450↓,
*Hif1a↓, In BV2 microglia, baicalein suppressed expression of hypoxia-induced HIF-1α and hypoxia responsive genes, including inducible nitric oxide synthase (iNOS), COX-2, and VEGF, by inhibiting ROS and PI3K/Akt pathway (Hwang et al. 2008).
*iNOS↓,
*COX2↓,
*VEGF↓,
*ROS↓,
*PI3K↓,
*Akt↓,
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Review, |
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AntiCan↓, anticancer, antidiabetic, antimicrobial, antiaging, neuroprotective, cardioprotective, respiratory protective, gastroprotective, hepatic protective, and renal protective effects
*neuroP↑,
*cardioP↑, Cardioprotective action of baicalein
*hepatoP↑,
*RenoP↑, baicalein’s capacity to lessen cisplatin-induced nephrotoxicity is probably due, at least in part, to the attenuation of renal oxidative and/or nitrative stress
TumCCA↑, Baicalein induces G1/S arrest in lung squamous carcinoma (CH27) cells by downregulating CDK4 and cyclin D1, as well as upregulating cyclin E
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↑,
BAX↑, SGC-7901 cells showed that when baicalein was administered, Bcl-2 was downregulated and Bax was increased
Bcl-2↓,
VEGF↓, Baicalein inhibits the synthesis of vascular endothelial growth factor (VEGF), HIF-1, c-Myc, and nuclear factor kappa B (NF-κB) in the G1 and S phases of ovarian cancer cell
Hif1a↓,
cMyc↓,
NF-kB↓,
ROS↑, Baicalein produced intracellular reactive oxygen species (ROS) and activated BNIP3 to slow down the development and hasten the apoptosis of MG-63,OS cell
BNIP3↑,
*neuroP↑, Baicalein exhibits neuroprotective qualities against amyloid (AN) functions by preventing AN from aggregating in PC12 neuronal cells to cause A𝛽-induced cytotoxicity
*cognitive↑, baicalein encourages non-amyloidogenic processing of APP, which lowers the generation of A𝛽 and enhances cognitive function
*NO↓, baicalein effectively reduced NO generation and iNOS gene expression
*iNOS↓,
*COX2↓, Baicalein therapy significantly decreased the expression of COX-2 and iNOS, as well as PGE2 and NF-κB, indicating a protective effect against cerebral I/R injury.
*PGE2↓,
*NRF2↑, Baicalein therapy markedly elevated nuclear Nrf2 expression and AMPK phosphorylation in the ischemic cerebral cortex
*p‑AMPK↑,
*Ferroptosis↓, Baicalein suppressed ferroptosis associated with 12/15-LOX, hence lessening the severity of post-traumatic epileptic episodes generated by FeCl3
*lipid-P↓, HT22 cells were damaged by ferroptosis, which is mitigated by baicalein may be due to its lipid peroxidation inhibitor
*ALAT↓, Baicalin lowers the raised levels of hepatic markers alanine transaminase (ALT), aspartate aminotransferase (AST)
*AST↓,
*Fas↓, Baicalin has also been shown to suppress apoptosis, decrease FAS protein expression, block the caspase-8 pathway, and decrease Bax protein production
*BAX↓,
*Apoptosis↓,
*tumCV↓,
*ROS↑,
*MMP↓,
*Fas↑,
*P53↑,
*P21↑,
*Bax:Bcl2↑,
*Casp3↑,
*Casp8↑,
*Casp9↑,
*cl‑PARP↑,
*TumCCA↑, S-phase cell cycle arrest
*P21↑,
*cycE/CCNE↑,
*cycA1/CCNA1↓,
*CDK2↓,
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in-vitro, |
Lung, |
H1299 |
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in-vitro, |
Lung, |
H460 |
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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↓,
AntiCan↑, The anticancer potential of lycopene has been described by various in vitro cells, animal studies, and some clinical trials.
antiOx↓, anticancer potential of lycopene is mainly due to its powerful singlet-oxygen quencher characteristics, simulation of detoxifying/antioxidant enzymes production,
Apoptosis↓, initiation of apoptosis, inhibition of cell proliferation and cell cycle progression as well as modulations of gap junctional communication, the growth factors, and signal transduction pathways
TumCP↓,
TumCCA↑,
Risk↓, The link between increased lycopene consumption and reducedoccurrence of a variety of cancers has been documented by in vitro cells,animal studies, and some clinical studies.
ROS↓, The antioxidant action of lycopene toward ROS
SOD↑, Lycopene can simulate detoxifying/antioxidant enzyme productionsuch as superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), and glutathione reductase.
Catalase↑, . By stimulating ARE system, the lycopene can increase detoxifying/antioxidant enzymes production such as SOD, CAT, GST
GSTs↑,
ARE↑, The upregulating of the ARE system by lycopere has been studied in human BEAS-2B, HepG2, and MCF7
NRF2↑, figure 1
cycD1/CCND1↓, figure 2
cycE/CCNE↑,
CDK2↑,
p27↑,
BAX↑,
Bcl-2↓,
P53↑,
ChemoSen↑, Lycopene has also been declared to have a synergistic effect with drugs used in cancer treatment [16,17,27,32]. Lycopene may contribute to improved anticancer effects of enzalutamide
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in-vitro, |
CRC, |
Caco-2 |
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in-vivo, |
Nor, |
HCEC 1CT |
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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.
Showing Research Papers: 1 to 6 of 6
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, ARE↑, 1, Catalase↑, 1, GSTs↑, 1, NRF2↑, 1, OXPHOS↑, 1, ROS↓, 1, ROS↑, 2, ROS⇅, 1, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↑, 1, OCR↑, 1,
Core Metabolism/Glycolysis ⓘ
12LOX↓, 1, cMyc↓, 2, ECAR↓, 1, Glycolysis↓, 1, lactateProd↓, 1, PDH↑, 1, PPP↓, 1,
Cell Death ⓘ
Apoptosis↓, 1, Apoptosis↑, 1, BAX↑, 2, Bcl-2↓, 2, Casp3↑, 1, Casp7↑, 1, Casp9↑, 1, Cyt‑c↑, 1, DR5↑, 1, MAPK↓, 1, p27↑, 2,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1,
Autophagy & Lysosomes ⓘ
BNIP3↑, 1,
DNA Damage & Repair ⓘ
P53↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK2↑, 1, CDK4↓, 3, cycA1/CCNA1↑, 1, cycD1/CCND1↓, 4, cycD1/CCND1↑, 1, CycD3↓, 1, cycE/CCNE↑, 5, P21↑, 1, TumCCA↑, 5,
Proliferation, Differentiation & Cell State ⓘ
ERK↓, 1, TumCG↓, 1,
Migration ⓘ
Ca+2↑, 1, Ca+2↝, 1, TumCP↓, 3,
Angiogenesis & Vasculature ⓘ
Hif1a↓, 2, VEGF↓, 2,
Immune & Inflammatory Signaling ⓘ
NF-kB↓, 2,
Hormonal & Nuclear Receptors ⓘ
CDK6↑, 1,
Drug Metabolism & Resistance ⓘ
BioEnh↑, 2, ChemoSen↑, 1, eff↑, 1, P450↓, 1,
Functional Outcomes ⓘ
AntiCan↓, 1, AntiCan↑, 1, Risk↓, 1,
Total Targets: 60
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
Ferroptosis↓, 1, lipid-P↓, 1, NRF2↑, 1, ROS↓, 1, ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↓, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, p‑AMPK↑, 1, ECAR∅, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↓, 1, BAX↓, 1, Bax:Bcl2↑, 1, Casp3↑, 1, Casp8↑, 1, Casp9↑, 1, Fas↓, 1, Fas↑, 1, Ferroptosis↓, 1, iNOS↓, 2,
Transcription & Epigenetics ⓘ
other?, 1, tumCV↓, 1,
DNA Damage & Repair ⓘ
P53↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, cycA1/CCNA1↓, 1, cycE/CCNE↑, 1, P21↑, 2, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
PI3K↓, 1,
Angiogenesis & Vasculature ⓘ
Hif1a↓, 1, NO↓, 1, VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, PGE2↓, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1,
Functional Outcomes ⓘ
cardioP↑, 1, cognitive↑, 1, hepatoP↑, 1, neuroP↑, 2, RenoP↑, 1,
Total Targets: 42
Scientific Paper Hit Count for: cycE/CCNE, Cyclin E
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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