S6K Cancer Research Results

S6K, S6 kinase: Click to Expand ⟱
Source:
Type: protein
S6K (S6 kinase) is a protein that plays a crucial role in cell growth, proliferation, and survival. It is a downstream target of the mTOR (mechanistic target of rapamycin) signaling pathway, which is a central regulator of cellular metabolism, growth, and division.

Research has shown that S6K is involved in the development and progression of various types of cancer, including breast, lung, prostate, and colon cancer. Overexpression or hyperactivation of S6K has been observed in many cancer types.
Scientific Papers found: Click to Expand⟱
2686- BBR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Nor, NA
Inflam↓, BBR has documented to have anti-diabetic, anti-inflammatory and anti-microbial (both anti-bacterial and anti-fungal) properties.
IL6↓, BBRs can inhibit IL-6, TNF-alpha, monocyte chemo-attractant protein 1 (MCP1) and COX-2 production and expression.
MCP1↓,
COX2↓,
PGE2↓, BBRs can also effect prostaglandin E2 (PGE2)
MMP2↓, and decrease the expression of key genes involved in metastasis including: MMP2 and MMP9.
MMP9↓,
DNAdam↑, BBR induces double strand DNA breaks and has similar effects as ionizing radiation
eff↝, In some cell types, this response has been reported to be TP53-dependent
Telomerase↓, This positively-charged nitrogen may result in the strong complex formations between BBR and nucleic acids and induce telomerase inhibition and topoisomerase poisoning
Bcl-2↓, BBR have been shown to suppress BCL-2 and expression of other genes by interacting with the TATA-binding protein and the TATA-box in certain gene promoter regions
AMPK↑, BBR has been shown in some studies to localize to the mitochondria and inhibit the electron transport chain and activate AMPK.
ROS↑, targeting the activity of mTOR/S6 and the generation of ROS
MMP↓, BBR has been shown to decrease mitochondrial membrane potential and intracellular ATP levels.
ATP↓,
p‑mTORC1↓, BBR induces AMPK activation and inhibits mTORC1 phosphorylation by suppressing phosphorylation of S6K at Thr 389 and S6 at Ser 240/244
p‑S6K↓,
ERK↓, BBR also suppresses ERK activation in MIA-PaCa-2 cells in response to fetal bovine serum, insulin or neurotensin stimulation
PI3K↓, Activation of AMPK is associated with inhibition of the PI3K/PTEN/Akt/mTORC1 and Raf/MEK/ERK pathways which are associated with cellular proliferation.
PTEN↑, RES was determined to upregulate phosphatase and tensin homolog (PTEN) expression and decrease the expression of activated Akt. In HCT116 cells, PTEN inhibits Akt signaling and proliferation.
Akt↓,
Raf↓,
MEK↓,
Dose↓, The effects of low doses of BBR (300 nM) on MIA-PaCa-2 cells were determined to be dependent on AMPK as knockdown of the alpha1 and alpha2 catalytic subunits of AMPK prevented the inhibitory effects of BBR on mTORC1 and ERK activities and DNA synthes
Dose↑, In contrast, higher doses of BBR inhibited mTORC1 and ERK activities and DNA synthesis by AMPK-independent mechanisms [223,224].
selectivity↑, BBR has been shown to have minimal effects on “normal cells” but has anti-proliferative effects on cancer cells (e.g., breast, liver, CRC cells) [225–227].
TumCCA↑, BBR induces G1 phase arrest in pancreatic cancer cells, while other drugs such as gemcitabine induce S-phase arrest
eff↑, BBR was determined to enhance the effects of epirubicin (EPI) on T24 bladder cancer cells
EGFR↓, In some glioblastoma cells, BBR has been shown to inhibit EGFR signaling by suppression of the Raf/MEK/ERK pathway but not AKT signaling
Glycolysis↓, accompanied by impaired glycolytic capacity.
Dose?, The IC50 for BBR was determined to be 134 micrograms/ml.
p27↑, Increased p27Kip1 and decreased CDK2, CDK4, Cyclin D and Cyclin E were observed.
CDK2↓,
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↓,
Bax:Bcl2↑, Increased BAX/BCL2 ratio was observed.
Casp3↑, The mitochondrial membrane potential was disrupted and activated caspase 3 and caspases 9 were observed
Casp9↑,
VEGFR2↓, BBR treatment decreased VEGFR, Akt and ERK1,2 activation and the expression of MMP2 and MMP9 [235].
ChemoSen↑, BBR has been shown to increase the anti-tumor effects of tamoxifen (TAM) in both drug-sensitive MCF-7 and drug-resistant MCF-7/TAM cells.
eff↑, The combination of BBR and CUR has been shown to be effective in suppressing the growth of certain breast cancer cell lines.
eff↑, BBR has been shown to synergize with the HSP-90 inhibitor NVP-AUY922 in inducing death of human CRC.
PGE2↓, BBR inhibits COX2 and PEG2 in CRC.
JAK2↓, BBR prevented the invasion and metastasis of CRC cells via inhibiting the COX2/PGE2 and JAK2/STAT3 signaling pathways.
STAT3↓,
CXCR4↓, BBR has been observed to inhibit the expression of the chemokine receptors (CXCR4 and CCR7) at the mRNA level in esophageal cancer cells.
CCR7↓,
uPA↓, BBR has also been shown to induce plasminogen activator inhibitor-1 (PAI-1) and suppress uPA in HCC cells which suppressed their invasiveness and motility.
CSCs↓, BBR has been shown to inhibit stemness, EMT and induce neuronal differentiation in neuroblastoma cells. BBR inhibited the expression of many genes associated with neuronal differentiation
EMT↓,
Diff↓,
CD133↓, BBR also suppressed the expression of many genes associated with cancer stemness such as beta-catenin, CD133, NESTIN, N-MYC, NOTCH and SOX2
Nestin↓,
n-MYC↓,
NOTCH↓,
SOX2↓,
Hif1a↓, BBR inhibited HIF-1alpha and VEGF expression in prostate cancer cells and increased their radio-sensitivity in in vitro as well as in animal studies [290].
VEGF↓,
RadioS↑,

2979- CUR,  GB,    Curcumin overcome primary gefitinib resistance in non-small-cell lung cancer cells through inducing autophagy-related cell death
- in-vitro, Lung, H157 - in-vitro, Lung, H1299
EGFR↓, Combination treatment with curcumin and gefitinib markedly downregulated EGFR activity through suppressing Sp1 and blocking interaction of Sp1 and HADC1,
Sp1/3/4↓,
ERK↓, and markedly suppressed receptor tyrosine kinases as well as ERK/MEK and AKT/S6K pathways in the resistant NSCLC cells.
MEK↓,
Akt↓,
S6K↓,

445- CUR,    Curcumin Regulates the Progression of Colorectal Cancer via LncRNA NBR2/AMPK Pathway
- in-vitro, CRC, HCT116 - in-vitro, CRC, HCT8 - in-vitro, CRC, SW480 - in-vitro, CRC, SW-620
p‑AMPK↑,
p‑ACC-α↑,
NBR2↑,
p‑S6K↓,
mTOR↓,

6695- DFC,    Inhibition of lactate dehydrogenase A by diclofenac sodium induces apoptosis in HeLa cells through activation of AMPK
- in-vitro, Cerv, HeLa
other↝, Cancer cells exhibit a unique metabolic preference for the glycolytic pathway over oxidative phosphorylation for maintaining the tumor microenvironment.
Glycolysis↓, Diclofenac (DCF), a nonsteroidal anti-inflammatory drug, has been shown to exhibit anticancer effects by interfering with the glucose metabolism pathway.
LDHA↓, DCF binds to LDHA adjacent to the substrate binding site and inhibits its activity in a dose-dependent and allosteric manner in HeLa cells.
Hypoxia↓, Thus, DCF inhibits the hypoxic microenvironment and induces apoptosis-mediated cell death.
Apoptosis↑,
lactateProd↓, DCF-induced LDHA inhibition alters pyruvate, lactate, NAD+, and ATP production in cells, and this could be a possible mechanism through which DCF inhibits glucose uptake in cancer cells.
ATP↓, DCF-induced ATP deprivation leads to mitochondria-mediated oxidative stress, which results in DNA damage, lipid peroxidation, and apoptosis-mediated cell death.
mt-ROS↑,
DNAdam↑,
lipid-P↑,
AMPK↑, Reduction in intracellular ATP levels additionally activates the sensor kinase, adenosine monophosphate-activated protein kinase (AMPK), which further downregulates phosphorylated ribosomal S6 kinase (p-S6K), leading to apoptosis-mediated cell death.
p‑S6K↓,
TumCP↓, DCF inhibits proliferation in HeLa cells
Dose↝, HeLa cells with an IC50 dose of 175 ± 4.86 μm on 24 h of incubation
selectivity↑, DCF did not significantly affect the viability of normal cervical cells at 175 μm (IC50 dose in HeLa cells), where the IC50 value was found to be greater than 1 mm concentration of DCF (
i-MDA↑, The result showed that DCF treatment in HeLa cells led to a significant increase in MDA levels, suggesting an increased level of lipid peroxidation
mtDam↑, Many reports suggest that there is a strong correlation between the inhibition of LDHA and the induction of oxidative stress (ROS production) via mitochondrial damage

959- PACs,    Grape seed extract inhibits VEGF expression via reducing HIF-1α protein expression
- in-vitro, GBM, U251 - in-vitro, BC, MDA-MB-231
Hif1a↓,
p‑Akt↓,
p‑S6K↓,
p‑S6↓,
VEGF↓,

1237- PTS,    Pterostilbene induces cell apoptosis and inhibits lipogenesis in SKOV3 ovarian cancer cells by activation of AMPK-induced inhibition of Akt/mTOR signaling cascade
- in-vitro, Ovarian, SKOV3
TumCMig↓,
TumCI↓,
MDA↑,
ROS↑,
BAX↑,
Casp3↑,
Bcl-2↓,
SREBP1↓,
FASN↓,
AMPK↓,
p‑AMPK↑,
p‑P53↑,
p‑TSC2↑,
p‑Akt↓,
p‑mTOR↓,
p‑S6K↓, p-S6K1
p‑4E-BP1↓,


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(tgid=1) ⓘ

lipid-P↑, 1,   MDA↑, 1,   i-MDA↑, 1,   ROS↑, 2,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 2,   MEK↓, 2,   MMP↓, 1,   mtDam↑, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

p‑ACC-α↑, 1,   AMPK↓, 1,   AMPK↑, 2,   p‑AMPK↑, 2,   FASN↓, 1,   Glycolysis↓, 2,   lactateProd↓, 1,   LDHA↓, 1,   p‑S6↓, 1,   S6K↓, 1,   p‑S6K↓, 5,   SREBP1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   p‑Akt↓, 2,   Apoptosis↑, 1,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Casp3↑, 2,   Casp9↑, 1,   p27↑, 1,   Telomerase↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Sp1/3/4↓, 1,   p‑TSC2↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 2,   NBR2↑, 1,   p‑P53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   TumCCA↑, 1,  

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

p‑4E-BP1↓, 1,   CD133↓, 1,   CSCs↓, 1,   Diff↓, 1,   EMT↓, 1,   ERK↓, 2,   mTOR↓, 1,   p‑mTOR↓, 1,   p‑mTORC1↓, 1,   n-MYC↓, 1,   Nestin↓, 1,   NOTCH↓, 1,   PI3K↓, 1,   PTEN↑, 1,   SOX2↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

MMP2↓, 1,   MMP9↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   uPA↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 2,   Hif1a↓, 2,   Hypoxia↓, 1,   VEGF↓, 2,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CCR7↓, 1,   COX2↓, 1,   CXCR4↓, 1,   IL6↓, 1,   Inflam↓, 1,   JAK2↓, 1,   MCP1↓, 1,   PGE2↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose?, 1,   Dose↓, 1,   Dose↑, 1,   Dose↝, 1,   eff↑, 3,   eff↝, 1,   RadioS↑, 1,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 2,   IL6↓, 1,  
Total Targets: 89

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: S6K, S6 kinase
2 Curcumin
1 Berberine
1 gefitinib, erlotinib
1 Diclofenac
1 Proanthocyanidins
1 Pterostilbene
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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