CDK6 Cancer Research Results
CDK6, Cyclin-dependent kinase 6: Click to Expand ⟱
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Cyclin-dependent kinase 6 (CDK6) is another important regulator of the cell cycle, particularly involved in the transition from the G1 phase to the S phase.
CDK6 is frequently overexpressed in various cancers, and its expression levels can serve as a prognostic marker. Targeting CDK6 with specific inhibitors, such as palbociclib (which also targets CDK4), has shown promise in clinical settings, particularly in hormone receptor-positive breast cancer.
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Scientific Papers found: Click to Expand⟱
TGF-β↓, Allicin can reduce the expression of TGF-2 and its receptor after entering directly into gastric cancer cell
cycD1/CCND1↓, followed by not only downexpression of cyclinD1, cyclinE, and cyclin-dependent kinase (CDK),
cycE/CCNE↓,
CDK1↓, cyclin-dependent kinase (CDK)
DNAdam↑, but also causing DNA damage and generating ROS
ROS↑,
BAX↑, Allicin increases the levels of Bax (proapoptotic protein), Bcl-2 (antiapoptotic protein), and JNK
JNK↑,
MMP↓, through reduction in outer mitochondrial membrane potential
p38↑, allicin induces p38 mitogen that could induce the protein kinase (MAPK) and then increase the expression of Fas binding to Fas ligand (Fas L) and finally activate death pathway through activation of cyt C and caspase-8.
MAPK↑,
Fas↑,
Cyt‑c↑,
Casp8↑,
PARP↑, allicin makes caspase-dependent apoptosis through elevating PARP, caspase-3 and caspase-9, which are mediated by enhanced discharging of mitochondria cyt C to the cytosol.
Casp3↑,
Casp9↑,
Ca+2↑, allicin induces apoptosis via increasing the amounts of free Ca2+, ER stress.
ER Stress↑,
P21↑, generating ROS to produce p21 and phospho-p53 (Ser15).
CDK2↓, Then p21 suppressed the CDK-4/6/cyclinD complex, P21-PCNA, P21-CDK2, and subsequently reduced cdk1/cyclinB1 complex for G2/M phase cell cycle arrest
CDK6↑,
TumCCA↑,
CDK4↓, Then p21 suppressed the CDK-4/6/cyclinD complex
TumCP↓, reported inhibitory effects on cancer cell proliferation, invasion and migration.
TumCI↓,
TumCMig↓,
Apoptosis↑, ART has been reported to induce apoptosis, differentiation and autophagy in colorectal cancer cells by impairing angiogenesis
Diff↑,
TumAuto↑,
angioG↓,
TumCCA↑, inducing cell cycle arrest (11), upregulating ROS levels, regulating signal transduction [for example, activating the AMPK-mTOR-Unc-51-like autophagy activating kinase (ULK1) pathway in human bladder cancer cells]
ROS↑,
AMPK↑,
mTOR↑,
ChemoSen↑, ART has been shown to restore the sensitivity of a number of cancer types to chemotherapeutic drugs by modulating various signaling pathways
Tf↑, ART could upregulate the mRNA levels of transferrin receptor (a positive regulator of ferroptosis), thus inducing apoptosis and ferroptosis in A549 non-small cell lung cancer (NSCLC) cells.
Ferroptosis↑,
Ferritin↓, ferritin degradation, lipid peroxidation and ferroptosis
lipid-P↑,
CDK1↑, Cyclin-dependent kinase 1, 2, 4 and 6
CDK2↑,
CDK4↑,
CDK6↑,
SIRT1↑, Sirt1 levels
COX2/PTGS2↓,
IL1β↓, IL-1? ?
survivin↓, ART can selectively downregulate the expression of survivin and induce the DNA damage response in glial cells to increase cell apoptosis and cell cycle arrest, resulting in increased sensitivity to radiotherapy
DNAdam↑,
RadioS↑,
Apoptosis↑,
TumCCA↓, CAPE (1-80 uM) can stimulate apoptosis and cell cycle arrest (G1 phase
TumCMig↓,
TumMeta↓,
ChemoSen↑,
eff↑, Nanoparticles promote therapeutic effect of CA and CAPE in reducing cancer cell malignancy.
eff↑, improve capacity of CA and CAPE in cancer suppression, it has been co-administered with other anti-tumor compounds such as gallic acid
eff↓, Currently, solvent extraction is utilized by methanol and ethyl acetate
combination at high temperatures. However, a low amount of CA is
yielded via this pathway
eff↝, Decyl CA (DCA) is a
novel derivative of CA but its role in affecting colorectal cancer has not
been completely understood.
Dose∅, The CAPE administration (0-60 uM) induces both
autophagy and apoptosis in C6 glioma cells.
AMPK↑, CAPE induces autophagy via AMPK upregulation.
p62↓, CAPE can induce autophagy via p62 down-regulation and LC3-II upregulation
LC3II↑,
Ca+2↑, CA (0-1000 uM) enhances Ca2+ accumulation in cells in a concentration-dependent manner
Bax:Bcl2↑, CA can promote Bax/Bcl-2 ratio i
CDK4↑, The administration of CAPE (1–80 μM)
can stimulate apoptosis and cell cycle arrest (G1 phase) via upregulation of Bax, CDK4, CDK6 and Rb
CDK6↑,
RB1↑,
EMT↓, CAPE has demonstrated high potential in inhibiting EMT in nasopharyngeal caner via enhancing E-cadherin levels, and reducing vimentin and β-catenin levels.
E-cadherin↑,
Vim↓,
β-catenin/ZEB1↓,
NF-kB↓,
angioG↑, CAPE (0.01-1ug/ml) inhibited angiogenesis via VEGF down-regulation
VEGF↓,
TSP-1↑, and furthermore, CAPE is capable of increasing TSP-1 levels
MMP9↓, CAPE was found to reduce MMP-9 expression
MMP2↓, CAPE can also down-regulate MMP-2
ChemoSen↑, role of CA and its derivatives in enhancing therapy sensitivity of cancer cells.
eff↑, CA administration (100 uM) alone or its combination with metformin (10 mM) can induce AMPK signaling
ROS↑, CA can promote ROS levels to induce cell death in human squamous cell carcinoma
CSCs↓, CA can reduce self-renewal capacity of CSCs and their migratory ability in vitro and in vivo.
Fas↑, CAPE (0-100 uM) is capable of inducing Fas signaling to promote p53 expression, leading to apoptotic cell death via Bax and caspase activation
P53↑,
BAX↑,
Casp↑,
β-catenin/ZEB1↓, anti-tumor activity of CAPE is mediated via reducing β-catenin levels
NDRG1↑, CAPE (30 uM) can promote NDRG1 expression via MAPK activation and down-regulation of STAT3
STAT3↓,
MAPK↑, CAPE stimulates mitogen-activated protein kinase (MAPK) and ERK
ERK↑,
eff↑, Res, thymoquinone and CAPE mediate lung tumor cell death via Bax
upregulation and Bcl-2 down-regulation.
eff↑, co-administration of CA (100 μM) and
metformin (10 mM) is of interest in cervical squamous cell carcinoma
therapy.
eff↑, in addition to CA, propolis contains other agents such as chrysin, p-coumaric acid and ferulic acid that are beneficial in tumor suppression.
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in-vitro, |
BC, |
SUM159 |
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in-vitro, |
BC, |
4T1 |
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PI3K↑, FMD activates PI3K-AKT, mTOR, and CDK4/6 as survival/growth pathways, which can be targeted by drugs to promote tumor regression.
Akt↑,
mTOR↑,
CDK4↑,
CDK6↑,
hyperG↓, FMD cycles also prevent hyperglycemia and other toxicities caused by these drugs.
TumCG↓, cycles of FMD significantly slowed down tumor growth, reduced tumor size, and caused an increased expression of intratumor Caspase3
TumVol↓,
Casp3↑,
BG↓, confirming our hypothesis that lowering intracellular glucose levels (through reduced extracellular levels or reduced uptake) reduces CSC survival
eff↑, 2DG potentiated the effect of FMD both in terms of delaying tumor progression and in decreasing the number of mammospheres derived by tumor masses,
eff∅, metformin did not show any additive or synergistic antitumor effect when combined with the FMD, thus suggesting that FMD and metformin have redundant effects on blood glucose levels
PKA↓, We have previously shown that prolonged fasting reduces the activity of protein kinase A (PKA) in different types of normal cells
KLF5↓, PKA inhibition resulted in the downregulation of KLF5, a potential therapeutic target for TNBC
p‑GSK‐3β↑, (GSK3β) phosphorylation
Nanog↓, stemness-associated genes NANOG and OCT4, and KLF2 and TBX3,
OCT4↓,
KLF2↓,
eff↑, Combining FMD cycles with PI3K/AKT/mTOR inhibitors results in long-term animal survival and reduces treatment-induced side effects
ROS↑, FMD resulted in an increased expression of pro-apoptotic molecules, such as BIM, and ASK1, a critical cellular stress sensor frequently activated by ROS, whose production was previously shown to be increased by the FMD
BIM↑,
ASK1↑,
PI3K↑, FMD cycles upregulate PI3K-AKT and mTOR pathways and downregulate CCNB-CDK1 while upregulating CCND-CDK4/6 signaling axes
Akt↑,
mTOR↑,
CDK1↓,
CDK4↑,
CDK6↑,
eff↑, combining STS with pictilisib, ipatasertib, and rapamycin, selective inhibitors for PI3K, AKT, and mTOR, respectively, resulted in enhanced cancer cell death and reduction of mammosphere numbers in SUM159 cells
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in-vitro, |
Pca, |
LNCaP |
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in-vitro, |
Pca, |
PC3 |
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in-vitro, |
Pca, |
22Rv1 |
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Dose↝, Treatment of fisetin (10–60 μM, 48 h) was found to result in a decrease in the viability of LNCaP, CWR22Rυ1 and PC-3 cells but had only minimal effects on normal prostate epithelial cells
tumCV↓,
selectivity↑,
TumCCA↑, Treatment of LNCaP cells with fisetin also resulted in G1-phase arrest that was associated with a marked decrease in the protein expression of cyclins D1, D2 and E
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↑, activating partner cyclin-dependent kinases 2, 4 and 6 with concomitant induction of WAF1/p21 and KIP1/p27.
CDK4↑,
CDK6↑,
P21↑,
p27/CDKN1B↑,
Apoptosis↑, Fisetin treatment also resulted in induction of apoptosis, poly (ADP-ribose) polymerase (PARP) cleavage
cl‑PARP↑,
Cyt‑c↑, induction of mitochondrial release of cytochrome c into cytosol, downregulation of X-linked inhibitor of apoptosis protein
XIAP↓,
Casp3↑, significant activation of caspases-3, -8 and -9
Casp8↑,
Casp9↑,
Bcl-2↓, In sharp contrast, the protein expression of Bcl-2 was significantly decreased by fisetin treatment in a dose-dependent fashion
PI3K↓, Inhibition of PI3K and phosphorylation of Akt protein expression by fisetin in LNCaP cells
Akt↓,
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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/CDKN1B↑,
ERK↓,
MAPK↓,
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Review, |
Var, |
NA |
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Review, |
IBD, |
NA |
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Review, |
Stroke, |
NA |
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Review, |
Sepsis, |
NA |
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Review, |
AD, |
NA |
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Dose↝, H2 can be administered exogenously and is also produced endogenously within the intestinal tract.
*Inflam↓, Anti‐Inflammatory Effect
*IL1β↓, diabetes combined with stroke, H₂ intervention downregulates the expression levels of proinflammatory factors (IL‐1β, IL‐6, TNF‐α), while activating the TLR4/NF‐κB signaling pathway to achieve neuroprotective effects
*IL6↓,
*TNF-α↓,
*neuroP↑,
*mTOR↓, sepsis model, H₂ regulates macrophage polarization (inhibiting the M1 phenotype/promoting the M2 phenotype) and inhibits (mTOR) phosphorylation, reducing the release of inflammatory mediators such as IL‐6, TNF‐α, and HMG
*IL10↑, while increasing the levels of anti‐inflammatory factors IL‐10 and Transforming Growth Factor‐beta (TGF‐β)
*TGF-β↑,
*Sepsis↓,
*NRF2↑, whereas Nrf2 induction suppresses these pathways via redox homeostasis modulation
*antiOx↑, figure 1
*Catalase↑,
*SOD↑,
*GPx↑,
*ROS↓, H₂ mediates ROS regulation through Nrf2, inhibiting NF‐κB/NLRP3 inflammasome activation and achieving an antioxidant–anti‐inflammatory synergistic effect
*HO-1↑, H2 can increase the expression of heme oxygenase‐1 (HO‐1) or activate the phosphatidylinositol‐3‐kinase (PI3K)–Akt signaling pathway to improve liver I/R injury
*PI3K↑,
*Akt↑,
*hepatoP↑,
*MPO↓, reduce myeloperoxidase (MPO) activity and IL‐1β/TNF‐α levels to alleviate myocardial injury
*cardioP↑,
CDK4↓, Studies have demonstrated that H2 inhibits CDK4 and CDK6 to restrict lung cancer progression
CDK6↑,
CD47↓, H₂ can reverse immune escape in lung cancer cells by inhibiting the expression of CD47 and activating the apoptosis program
PI3K↓, H2 promotes apoptosis by downregulating Akt phosphorylation and inhibiting the PI3K signaling pathway in non‐small cell lung cancer.
Akt↓,
Hif1a↓, inhalation of H2 suppresses Hypoxia‐Inducible Factor 1 Alpha Subunit (HIF‐1α)/NF‐κB signaling pathway activation and promotes apoptosis in HeLa cells
selectivity↑, This bidirectional regulatory capability allows H₂ to protect normal tissues from excessive apoptosis (such as inflammation‐induced cell death) while selectively inducing apoptosis in tumor cells.
*MMP↑, howed that after treating septic rats with HRS, the decline in mitochondrial membrane potential (MMP) and ATP content was improved.
*ATP↑,
*ER Stress↓, H₂ alleviated inflammation and organ damage by inhibiting ER stress and activating the autophagy pathway in septic mice
*CHOP/DDIT3↓, H2 could downregulate the expression of CHOP, caspase‐12, and GRP78, while inhibiting p38 and c‐Jun N‐terminal kinase (JNK) phosphorylation, and upregulating the LC3‐II/I ratio
*Casp12↓,
*GRP78/BiP↓,
*p38↓,
*p‑JNK↓,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p‑eIF2α↓, HRW prevents IBD in mice by reducing levels of p‐eIF2α, ATF4, XBP1, and CHOP, key proteins in ER stress.
*ATF4↓,
*XBP-1↓,
*Imm↑, H₂ exhibit multidimensional characteristics, primarily enhancing immunity by protecting immune organs,
*IFN-γ↓, H2 treatment inhibited several T‐cell effector molecules, such as IFN‐γ, IL‐4, and GZMB
*IL4↓,
*GranB/GZMB↓,
NK cell↑, After inhaling H₂ for 2 weeks, patients with advanced non‐small cell lung cancer showed significant improvement in T‐cell exhaustion. (NK) subgroups was higher than the pretreatment percentag
radioP↑, HRS can protect against radiation‐induced immune dysfunction by restoring the number of CD4+ T and CD8+ T cells in the spleen.
*CD4+↑,
CD8+↑,
*Dose↝, Common delivery methods include inhalation, oral administration of HRW, injection of HRS, promotion of endogenous H2 production
*other↑, H2, which fall within the explosive range at concentrations ranging from 4 to 74%, it is essential to specify the concentration of H2 for inhalation therapy.
*Dose↝, China National Health Commission recommends the administration of oxygen–H2 mixture (33.3% O2 and 66.6% H2)
*antiPs↑, HRW baths exhibit inhibitory effects on inflammation and oxidative stress while demonstrating therapeutic benefits for conditions such as psoriasis
*BioAv↝, the solubility of H2 in water at room temperature and pressure is limited to a maximum of 0.8mM109, resulting in limited efficacy when orally administered.
*GutMicro↑, inhalation of H2 modulates the gut flora to ameliorate acute alcoholic liver injury. H2 altered the composition of the GM, leading to an increase in the relative abundance of Mycobacterium anisopliae and Mycobacterium thickum
Dose↝, CRC cell lines (ROK/SW480/HCT116) and xenograft mouse models,Inhalation of 66% H2 (66% H2 and 33% O2);Duration: 2 h a day for 21 days
*IBI↑, orally administered silicon H2 nanoparticles (SiH NPs) for targeted scavenging of ROS at inflammatory sites, thereby alleviating symptoms of IBD and restoring GM diversity by enhancing the abundance of beneficial bacteria.
TumCP↓, H2 inhibits tumor cell activity, proliferation, invasion, and migration through various molecular mechanisms, in a manner that depends on both dose and time.
TumCI↓,
TumCMig↓,
CD8+↑, H2 Improves Prognosis by Restoring Depleted CD8+ T Cells in Patients with CRC Cancer
PGC-1α↑, It has been shown that H2 can activate PGC‐1α to restore mitochondrial function and rescue depleted CD8+T cells
Akt↓, H2 Inhibits CRC Cell Proliferation by Suppressing the AKT/SCD1 Pathway
SCD1↓,
*MDA↓, The results showed that H2 water alone significantly improved detected antioxidant markers (SOD and CAT) and reduced MDA levels.
eff↑, combination of H2 water and 5‐fluorouracil significantly attenuated MDA levels more effectively than 5‐fluorouracil alone
*APP↓, H2 gas significantly inhibited the overexpression of APP, BACE1, and sAP, thereby reducing Aβ production.
*BACE/β-secretase↓,
*Aβ↓,
*cognitive↑, This intervention effectively halted the progression of AD, alleviating cognitive impairment, synaptic deficits, and neuronal death
*neuroP↑, regulation of GM(gutmicrobiome) by HRW considered a key mechanism underlying its neuroprotective effects.
NP/CIPN↓, mice with chemotherapy‐induced neuropathic pain caused by oxaliplatin, drinking HRW significantly reduced inflammation by inhibiting the LPS–TLR4 pathway and decreasing the expression of TNF‐α and IL‐6.
*Stroke↓, inhalation of 2% H2 gas significantly reduced levels of myocardial injury markers, such as creatine kinase‐MB and cardiac troponin‐T, while protecting myocardial tissue from further damage by inhibiting autophagy.
*NLRP3↓, daily inhalation of 2% H2 gas for 3 h over 28 days effectively suppressed the activation of the NLRP3 inflammasome, reduced cardiac fibrosis, and improved cardiac function
*ALAT↓, 4% H2 outperforming 67% H2 in reducing liver enzyme levels Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and lipid accumulation.
*AST↓,
*LPS↓, inhalation of 4% H2 in an NAFLD rat model significantly lowered plasma LPS levels, inhibited the LPS/TLR4/NF‐κB signaling pathway to reduce liver inflammation
*hepatoP↑, drinking HRW, indicating its hepatoprotective effects
chemoP↑, injecting HRS in rats effectively reduced ALT and AST levels caused by doxorubicin, decreased ROS and MDA production, and regulated the Bax/Bcl‐2 ratio to alleviate inflammation and apoptosis.
*creat↓, mouse model of kidney injury induced by a high‐oxalate diet, HRW consumption markedly improved serum creatinine, blood urea nitrogen, and kidney injury markers such as kidney injury molecule‐1 (KIM‐1)
*Urea↓,
*RenoP↑,
*eff↑, higher concentrations of H2 gas (67%) produced more pronounced improvements in kidney histology and morphology compared with lower concentrations (4%)
Apoptosis↑, H2 gas increased apoptosis in A549 cells while reducing the expression of XIAP and BIRC3 proteins in studies on A549 cells and their nude mouse models.
XIAP↓,
IAP2/BIRC3↓,
TumVol↓, inhalation of 60% H2 gas significantly reduced tumor volume in experimental mice
MALAT1↓, In gastric cancer research, Zhu et al. [10] found that H2 gas downregulated the expression of lncRNA MALAT1 and EZH2 while upregulating miR‐124‐3p
EZH2↓,
miR-124-3p↓,
eff↑, combining platinum nanocolloid (Pt‐nc) with H2 gas effectively inhibited the growth of human promyelocytic leukemia HL60 cells
ChemoSen↑, combining H2 therapy with conventional treatments such as chemotherapy and radiotherapy, demonstrating improved efficacy and reduced side effects
*compII↑, allergic airway inflammation, showing that H2 increased ATP production as well as the activity of mitochondrial respiratory chain complexes I and III
*compIII↑,
*LDL↓, H2‐enriched water in humans, showing that supplementation with H2‐enriched water appeared to reduce serum low‐density lipoprotein cholesterol (LDL‐C) and apolipoprotein B (apoB) levels,
*Obesity↓, H2 may play a beneficial role in the prevention of potential metabolic syndrome
QoL↑, 82 patients with stage III and IV cancers receiving H2 inhalation therapy. They found that H2 inhalation improved the quality of life
PFS↑, Sixteen months of follow‐up found that progression‐free survival in the control group was lower than that in the H2 inhalation group alone, and significantly lower than that in the other three combination therapy groups.
Showing Research Papers: 1 to 7 of 7
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
CD47↓, 1, miR-124-3p↓, 1, PFS↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
Ferroptosis↑, 1, hyperG↓, 1, lipid-P↑, 1, ROS↑, 4,
Metal & Cofactor Biology(tgid=2) ⓘ
Ferritin↓, 1, KLF5↓, 1, Tf↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 1, PGC-1α↑, 1, XIAP↓, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 2, SCD1↓, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 3, Akt↑, 2, Apoptosis↑, 4, ASK1↑, 1, BAX↑, 2, Bax:Bcl2↑, 1, Bcl-2↓, 1, BIM↑, 1, Casp↑, 1, Casp3↑, 3, Casp8↑, 2, Casp9↑, 2, Cyt‑c↑, 2, Fas↑, 2, Ferroptosis↑, 1, IAP2/BIRC3↓, 1, JNK↑, 1, MAPK↓, 1, MAPK↑, 2, p27/CDKN1B↑, 2, p38↑, 1, survivin↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
EZH2↓, 1, tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LC3II↑, 1, p62↓, 1, TumAuto↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 2, P53↑, 1, PARP↑, 1, cl‑PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 2, CDK1↑, 1, CDK2↓, 2, CDK2↑, 2, CDK4↓, 3, CDK4↑, 5, cycD1/CCND1↓, 3, CycD3↓, 1, cycE/CCNE↓, 2, cycE/CCNE↑, 1, P21↑, 3, RB1↑, 1, TumCCA↓, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CSCs↓, 1, Diff↑, 1, EMT↓, 1, ERK↓, 1, ERK↑, 1, p‑GSK‐3β↑, 1, mTOR↑, 3, Nanog↓, 1, OCT4↓, 1, PI3K↓, 2, PI3K↑, 2, STAT3↓, 1, TumCG↓, 1,
Migration(tgid=13) ⓘ
Ca+2↑, 2, E-cadherin↑, 1, KLF2↓, 1, MALAT1↓, 1, MMP2↓, 1, MMP9↓, 1, PKA↓, 1, TGF-β↓, 1, TSP-1↑, 1, TumCI↓, 2, TumCMig↓, 3, TumCP↓, 3, TumMeta↓, 1, Vim↓, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, angioG↑, 1, Hif1a↓, 1, VEGF↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, IL1β↓, 1, NF-kB↓, 1, NK cell↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↑, 8,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 4, Dose↝, 3, Dose∅, 1, eff↓, 1, eff↑, 11, eff↝, 1, eff∅, 1, RadioS↑, 1, selectivity↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
BG↓, 1, EZH2↓, 1, Ferritin↓, 1,
Functional Outcomes(tgid=23) ⓘ
chemoP↑, 1, NDRG1↑, 1, NP/CIPN↓, 1, QoL↑, 1, radioP↑, 1, TumVol↓, 2,
Infection & Microbiome(tgid=24) ⓘ
CD8+↑, 2,
Total Targets: 118
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
compII↑, 1, Stroke↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, Catalase↑, 1, GPx↑, 1, HO-1↑, 1, MDA↓, 1, MPO↓, 1, NRF2↑, 1, ROS↓, 1, SOD↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, compIII↑, 1, MMP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, LDL↓, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 1, Casp12↓, 1, GranB/GZMB↓, 1, p‑JNK↓, 1, p38↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↓, 1, p‑eIF2α↓, 1, ER Stress↓, 1, GRP78/BiP↓, 1, XBP-1↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LC3‑Ⅱ/LC3‑Ⅰ↑, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
mTOR↓, 1, PI3K↑, 1,
Migration(tgid=13) ⓘ
APP↓, 1, TGF-β↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
ATF4↓, 1,
Barriers & Transport(tgid=15) ⓘ
IBI↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↑, 1, IFN-γ↓, 1, IL10↑, 1, IL1β↓, 1, IL4↓, 1, IL6↓, 1, Imm↑, 1, Inflam↓, 1, LPS↓, 1, TNF-α↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 1, BACE/β-secretase↓, 1, NLRP3↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↝, 1, Dose↝, 2, eff↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, AST↓, 1, creat↓, 1, GutMicro↑, 1, IL6↓, 1, Urea↓, 1,
Functional Outcomes(tgid=23) ⓘ
antiPs↑, 1, cardioP↑, 1, cognitive↑, 1, hepatoP↑, 2, neuroP↑, 2, Obesity↓, 1, RenoP↑, 1,
Infection & Microbiome(tgid=24) ⓘ
Sepsis↓, 1,
Total Targets: 64
Scientific Paper Hit Count for: CDK6, Cyclin-dependent kinase 6
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#:895 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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