Cyc Cancer Research Results
Cyc, Cyclin: Click to Expand ⟱
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Cyclins are indispensable elements of the cell cycle and derangement of their function can lead to cancer formation.
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
Liver, |
HepG2 |
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in-vitro, |
Liver, |
FaO |
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Cyc↓, cyclin A
P21↑,
ROS↑, α-LA treatment at a concentration that induces apoptosis (500 µM) caused increased ROS generation in FaO cells, as early as 1 h after treatment with a further increase at 3 and 6 h.
p‑P53↑,
BAX↑, 500 µM α-LA produced an increase in Bax levels as early as 24 h
Cyt‑c↑, release from mitochondria
Casp↑, Treatment of HepG2 cells with 500 µM α-LA caused a time-dependent activation of caspase-3, as indicated by a progressive decrease of levels of pro-caspase-3
survivin↓,
JNK↑,
Akt↓,
Bcl-2↓,
survivin↓,
Casp8↑,
P53↑,
Sharpin↓,
APAF1↑,
p‑Akt↓,
NF-kB↓,
P21↑,
Cyc↓,
CDK2↓,
CDK4/6↓,
Snail↓,
ChemoSen↑, Apigenin significantly increased the inhibitory effects of cisplatin on cell migration via downregulation of Snail expression
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in-vitro, |
BC, |
MDA-MB-231 |
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Cyc↓, Cyclin A
CycB/CCNB1↓,
CDK1↓,
P21↑,
PCNA↝,
HDAC↓, apigenin treatment for 48 h suppressed HDAC activity in MDA-MB-231 cells in a dose-dependent manner
TumCP↓, Apigenin Inhibited MDA-MB-231 Cell Proliferation
TumCCA↑, Apigenin Induced G2/M Arrest in MDA-MB-231 Cells
ac‑H3↑, H3 acetylation increased in time-dependent
TumW↓, apigenin treatment significantly reduced the
tumor volume and tumor weight
TumVol↓,
CDK1↓, graphical abstract
Cyc↓,
p27↑,
P21↑,
P53↑,
TumCCA↑, Cell cycle arrest
TumCI↓, Inhibit invastion
MMP2↓,
MMP9↓,
E-cadherin↑,
N-cadherin↓,
Vim↓,
LC3A↑,
p62↓,
p‑mTOR↓,
PD-L1↓,
CAFs/TAFs↓,
VEGF↓,
ROCK1↓,
Bcl-2↓,
Bcl-xL↓,
BAX↑,
ROS↑,
cl‑PARP↑,
Casp3↑,
Casp9↑,
PTEN↑, A549, H460
MMP↓, ↓mitochondrial transmembrane potential, redistribution of cytochrome c,
Cyt‑c↑,
Ca+2↑, ↑Ca2+
PERK↑, ↑PERK, ↑IRE1α, ↑CHOP,
IRE1↑,
CHOP↑,
Copper↑, ↑Cu+2
Snail↓, ↓Snail, ↓vimentin, ↓Twist1,
Vim↓,
Twist↓,
GSH↓, ↑ROS, ↓GSH, ↑MDA, ↓MMP, ↓NRF2, ↓HO-1, ↓GPX4, ↓FTH1, ↑TFR1, ↓p-JAK2, ↓p-STAT3
NRF2↓,
HO-1↓,
GPx4↓,
XIAP↓, ↓Bcl-2, ↓Bcl-xL, ↓XIAP, ↓surviving
survivin↓,
DR5↑, ↑ROS, ↑DR5
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in-vitro, |
neuroblastoma, |
NA |
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CSCs↓, Berberine attenuated cancer stemness markers CD133, β-catenin, n-myc, sox2, notch2 and nestin.
CD133↓,
β-catenin/ZEB1↓,
n-MYC↓,
SOX2↓,
NOTCH2↓,
Nestin↓,
TumCCA↑, Berberine potentiated G0/G1 cell cycle arrest by inhibiting proliferation, cyclin dependent kinases and cyclins resulting in apoptosis through increased bax/bcl-2 ratio.
TumCP↓,
CDK1↓,
Cyc↓,
Apoptosis↑,
Bax:Bcl2↑,
NCAM↓, The induction of NCAM and reduction in its polysialylation indicates anti-migratory potential which is supported by down regulation of MMP-2/9.
MMP2↓,
MMP9↓,
*Smad1↑, It increased epithelial marker laminin and smad and increased Hsp70 levels also suggest its protective role.
*HSP70/HSPA5↑,
*LAMs↑,
TumCP↓, Betulinic acid (BA), a pipeline anticancer drug, exerts anti-proliferative effects on breast cancer cells is mainly through inhibition of cyclin and topoisomerase expression, leading to cell cycle arrest.
Cyc↓,
TOP1↓,
TumCCA↑,
angioG↓, anti-angiogenesis effect by inhibiting the expression of transcription factor nuclear factor kappa B (NF-κB), specificity protein (Sp) transcription factors, and vascular endothelial growth factor (VEGF) signaling.
NF-kB↓, Inhibition of NF-kB signaling pathway
Sp1/3/4↓,
VEGF↓,
MMPs↓, inhibiting the expression of matrix metalloproteases
ChemoSen↑, Synergistically interactions of BA with other chemotherapeutics are also described in the literature.
eff↑, BA is highly lipid soluble [74,75], and it readily passes through membranes, including plasma and mitochondrial membranes. BA
acts directly on mitochondria
MMP↓, decreases mitochondrial outer membrane potential (MOMP), leading to increased outer membrane permeability, generation of reactive oxygen species (ROS),
ROS↑,
Bcl-2↓, reducing expression of anti-apoptotic proteins Bcl-2, Bcl-XL and Mcl-1
Bcl-xL↓,
Mcl-1↓,
lipid-P↑, BA inhibits the growth of breast cancer cells via lipid peroxidation resulting from the generation of ROS
RadioS↑, The cytotoxicity effect of BA on glioblastoma cells is not strong; however, some studies indicate that the combination of BA and radiotherapy could represent an advancement in treatment of glioblastoma [
eff↑, BA and thymoquinone inhibit MDR and induce cell death in MCF-7 breast cancer cells by suppressing BCRP [
*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
Cyc↓, dose-dependent reduction in cyclins A–E
MAPK↓,
TumCMig↓,
LAMP2↓,
p‑ERK⇅, Phosphorylated ERK (P-ERK1/2) increased at intermediate exposures (100 and 250 μM), relative to control, but was reduced by higher concentrations of BA
TumCM/A↑, BA induces media acidosis
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↓,
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in-vitro, |
NMSC, |
A431 |
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in-vitro, |
NMSC, |
UW-BCC1 |
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in-vitro, |
Nor, |
NHEKn |
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TumCG↓,
TumCCA↑, induce G0/G1 cell cycle arrest
Cyc↓,
Apoptosis↑,
cl‑Casp3↑,
cl‑Casp8↑,
cl‑PARP↑,
HH↓,
Smo↓,
Gli1↓,
GLI2↓,
Shh↓,
Sufu↑,
BAX↑,
Bcl-2↓,
*toxicity↓, normal cells 10-fold higher IC50
*BioAv↓, Hydroxycinnamic acids are sensitive compounds to the environment in the gastrointestinal track. They may interact with the components in the digestion system or can be affected by pH differences
Inflam↓, Hydroxycinnamic acids (p-coumaric, CAPE, chlorogenic, caffeic, and ferulic acids) exhibit anti-inflammatory activity both in vitro and in vivo
COX2↓, caffeic acid targets COX-2 and its product prostaglan-din E2
TumCCA↑, These phenolics can cause cell cycle arrest at various phases, including G1, S, S-G2, and G2.
ChemoSen↑, sensitize cancer cells to chemotherapy and radiation therapy.
RadioS↑,
selectivity↑, HCAs exhibit selective toxicity, with a higher propensity to induce cell death in cancerous cells compared to normal cells.
ROS↑, 100uM(CA) and 10mM(metforin) cervical Cancer, also 100uM@24hr in A549cells
DNAdam↑,
antiOx↑, Hydroxy-cinnamic acids have an antioxidant effect by suppressing reactive oxygen/nitrogen species (ROS/RNS) and superoxide dismutases (SODs) production
SOD↑,
Catalase↑,
GPx↑,
GSH↑,
NRF2↑,
NF-kB↓, In the promotion stage, these compounds possess anti-inflammatory effects, particularly by inhibit-ing nuclear factor kappa B (NF-kB)
Cyc↓,
CDK1↑, CDKs
P21↑,
p27↑,
P53↑,
VEGF↓,
MAPK↓,
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in-vitro, |
GBM, |
U87MG |
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NA, |
AD, |
NA |
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in-vitro, |
GBM, |
A172 |
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in-vitro, |
GBM, |
T98G |
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Warburg↓, Here, we documented that methylene blue (MB) reverses the Warburg effect evidenced by the increasing of oxygen consumption and reduction of lactate production in GBM cell lines
OCR↑, increases cellular oxygen consumption, and decreases lactate production in murine hippocampal cells
lactateProd↓,
TumCP↓, MB decreases GBM cell proliferation and halts the cell cycle in S phase.
TumCCA↑,
AMPK↑, Through activation of AMP-activated protein kinase, MB inactivates downstream acetyl-CoA carboxylase and decreases cyclin expression.
ACC↓,
Cyc↓,
neuroP↑, There is mounting evidence that MB enhances brain metabolism and exerts neuroprotective effects in multiple neurodegenerative disease models including Parkinson, Alzheimer, and Huntington disease
Cyt‑c↝, MB has long been known as an electron carrier, which is best represented by MB ability to increase the rate of cytochrome c reduction in isolated mitochondria
Glycolysis↓, MB Decreases Aerobic Glycolysis in U87 Cells
ECAR↓, MB increases OCR and decreases ECAR in U87 cells
TumCG↓, MB Inhibits Tumor Growth in Vitro
other↓, MB dramatically inhibits expression of cyclin A2, B1,and D1 while having less effect on cyclin E1
Showing Research Papers: 1 to 12 of 12
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, Catalase↓, 1, Catalase↑, 1, Copper↑, 1, GPx↑, 1, GPx4↓, 1, GSH↓, 2, GSH↑, 1, HO-1↓, 1, lipid-P↑, 1, MDA↑, 1, NRF2↓, 1, NRF2↑, 2, ROS↑, 5, SAM-e↝, 1, SOD↓, 1, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
p‑MEK↓, 1, MMP↓, 2, OCR↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
ACC↓, 1, AMPK↑, 1, ECAR↓, 1, Glycolysis↓, 1, lactateProd↓, 1, NAD↝, 1, PI3K/Akt↝, 1, TumCM/A↑, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↓, 1, p‑Akt↓, 1, APAF1↑, 1, Apoptosis↑, 3, BAX↑, 4, Bax:Bcl2↑, 1, Bcl-2↓, 5, Bcl-xL↓, 3, BID↑, 1, Casp↑, 1, Casp3↑, 2, cl‑Casp3↑, 1, Casp8↑, 1, cl‑Casp8↑, 1, Casp9↑, 2, Cyt‑c↑, 2, Cyt‑c↝, 1, DR5↑, 1, JNK↑, 1, MAPK↓, 2, MAPK↝, 1, Mcl-1↓, 1, p27↑, 2, survivin↓, 3,
Kinase & Signal Transduction ⓘ
Sp1/3/4↓, 1,
Transcription & Epigenetics ⓘ
ac‑H3↑, 1, other↓, 1,
Protein Folding & ER Stress ⓘ
ATF6↑, 1, CHOP↑, 1, eIF2α↑, 1, IRE1↑, 1, PERK↑, 1,
Autophagy & Lysosomes ⓘ
LAMP2↓, 1, LC3A↑, 1, p62↓, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1, P53↑, 3, p‑P53↑, 1, cl‑PARP↑, 2, PCNA↝, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 3, CDK1↑, 1, CDK2↓, 1, Cyc↓, 12, CycB/CCNB1↓, 1, P21↓, 1, P21↑, 5, TumCCA↑, 7,
Proliferation, Differentiation & Cell State ⓘ
BRAF↝, 1, CD133↓, 1, CSCs↓, 1, p‑ERK↓, 1, p‑ERK⇅, 1, Gli1↓, 1, HDAC↓, 2, HH↓, 1, IGF-1↓, 2, p‑mTOR↓, 1, n-MYC↓, 1, Nestin↓, 1, NOTCH2↓, 1, PTEN↑, 1, PTEN↝, 1, Shh↓, 1, Smo↓, 1, SOX2↓, 1, Sufu↑, 1, TOP1↓, 1, TumCG↓, 2,
Migration ⓘ
Ca+2↑, 1, CAFs/TAFs↓, 1, CDK4/6↓, 1, E-cadherin↑, 1, GLI2↓, 1, MMP2↓, 2, MMP9↓, 2, MMPs↓, 1, N-cadherin↓, 1, NCAM↓, 1, ROCK1↓, 1, Sharpin↓, 1, Snail↓, 2, TumCI↓, 1, TumCMig↓, 2, TumCP↓, 4, Twist↓, 1, Vim↓, 2, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, ATF4↑, 1, HIF-1↓, 1, VEGF↓, 3,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL1↓, 1, IL6↓, 1, Inflam↓, 1, NF-kB↓, 3, PD-L1↓, 1, PSA↓, 2, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 3, eff↑, 2, RadioS↑, 2, selectivity↑, 1,
Clinical Biomarkers ⓘ
BRAF↝, 1, IL6↓, 1, PD-L1↓, 1, PSA↓, 2,
Functional Outcomes ⓘ
AntiCan↑, 1, neuroP↑, 1, Risk↓, 1, TumVol↓, 2, TumW↓, 1,
Total Targets: 143
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
Catalase↑, 1, GPx↑, 1, SAM-e↑, 1, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↝, 1,
Core Metabolism/Glycolysis ⓘ
NAD↝, 1,
Protein Folding & ER Stress ⓘ
HSP70/HSPA5↑, 1,
Migration ⓘ
Ca+2↝, 1, LAMs↑, 1, serineP↓, 1, Smad1↑, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1, TNF-α↓, 1, VitD↑, 1,
Hormonal & Nuclear Receptors ⓘ
testos↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, Dose↑, 1, Dose↝, 1, eff↑, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
BMD↑, 1, BMPs↑, 1, Calcium↑, 1, hs-CRP↓, 1, Mag↑, 1, VitD↑, 1,
Functional Outcomes ⓘ
chemoP↑, 1, chemoPv↑, 1, ChemoSideEff↓, 1, cognitive↑, 1, memory↑, 1, neuroP↑, 1, Risk↓, 1, toxicity↓, 1,
Total Targets: 34
Scientific Paper Hit Count for: Cyc, Cyclin
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#:374 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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