p70S6 Cancer Research Results

p70S6, phospho-S6: Click to Expand ⟱
Source:
Type:
p70S6, also known as phospho-S6, is the phosphorylated form of the S6 protein, which is a component of the 40S ribosomal subunit. The S6 protein is a key regulator of protein synthesis, and its phosphorylation by p70S6K is a critical event in the regulation of translation.
Overexpressed in: breast, prostate, lung CRC pancreatic, ovarian, Melanoma, HCC, RCC, throid, Esophageal, stomach.
Scientific Papers found: Click to Expand⟱
1008- Api,    Apigenin-induced lysosomal degradation of β-catenin in Wnt/β-catenin signaling
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW480
Wnt/(β-catenin)↓,
β-catenin/ZEB1↓,
TumAuto↑,
Akt↓,
mTOR↓,
tumCV↓,
TumCCA↑, cell cycle arrest at G2/M phase
TumAuto↑, data suggested the involvement of autophagy in apigenin-induced β-catenin down-regulation during Wnt signaling
p‑Akt↓,
p‑p70S6↓,
p‑4E-BP1↓,

1357- Ash,    Cytotoxicity of withaferin A in glioblastomas involves induction of an oxidative stress-mediated heat shock response while altering Akt/mTOR and MAPK signaling pathways
- in-vitro, GBM, U87MG - in-vitro, GBM, U251 - in-vitro, GBM, GL26
TumCP↓,
TumCCA↑, G2/M cell cycle
Akt↓,
mTOR↓,
p70S6↓,
p85S6K↓,
AMPKα↑,
TSC2↑,
HSP70/HSPA5↑,
HO-1↑,
HSF1↓,
Apoptosis↑,
ROS↑, Withaferin A elevates pro-oxidant potential in GBM cells and induces a cellular oxidative stress response
eff↓, Pre-treatment with a thiol-antioxidant protects GBM cells from the anti-proliferative and cytotoxic effects of withaferin A NAC pretreatment was able to completely prevent cell cycle shift to G2/M arrest following 1µM WA treatment at 24h

750- Bor,    Calcium fructoborate regulate colon cancer (Caco-2) cytotoxicity through modulation of apoptosis
- in-vitro, CRC, Caco-2
Bcl-2↓,
BAX↑,
Akt↓,
p70S6↓,
PTEN↑,
TSC2↑,

2792- CHr,    Chrysin induces death of prostate cancer cells by inducing ROS and ER stress
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3
DNAdam↑, chrysin induced apoptosis of cells evidenced by DNA fragmentation and increasing the population of both DU145 and PC-3 cells in the sub-G1 phase of the cell cycle
TumCCA↑,
MMP↓, chrysin induced loss of mitochondria membrane potential (MMP), while increasing production of reactive oxygen species (ROS) and lipid peroxidation in a dose-dependent manner
ROS↑,
lipid-P↑,
ER Stress↑, Also, it induced endoplasmic reticulum (ER) stress through activation of unfolded protein response (UPR) proteins including PRKR-like ER kinase (PERK), eukaryotic translation initiation factor 2α (eIF2α), and 78 kDa glucose-regulated protein (GRP78)
UPR↑,
PERK↑,
eIF2α↑,
GRP78/BiP↑,
PI3K↓, chrysin-mediated intracellular signaling pathways suppressed phosphoinositide 3-kinase (PI3K) and the abundance of AKT, P70S6K, S6, and P90RSK proteins, but stimulated mitogen-activated protein kinases (MAPK) and activation of ERK1/2 and P38 proteins
Akt↓,
p70S6↓,
MAPK↑,

463- CUR,    Curcumin induces autophagic cell death in human thyroid cancer cells
- in-vitro, Thyroid, K1 - in-vitro, Thyroid, FTC-133 - in-vitro, Thyroid, BCPAP - in-vitro, Thyroid, 8505C
TumAuto↑,
LC3II↑,
Beclin-1↑,
p‑p38↑,
p‑JNK↑,
p‑ERK↑, p-ERK1/2
p62↓,
p‑PDK1↓,
p‑Akt↓,
p‑p70S6↓,
p‑PIK3R1↓,
p‑S6↓,
p‑4E-BP1↓,

948- F,    Low Molecular Weight Fucoidan Inhibits Tumor Angiogenesis through Downregulation of HIF-1/VEGF Signaling under Hypoxia
- vitro+vivo, Bladder, T24/HTB-9 - in-vitro, Nor, HUVECs
p‑PI3k/Akt/mTOR↓,
p‑p70S6↓,
p‑4E-BP1↓,
angioG↓, did not affect angiogenesis under normoxic conditions (data not shown), suggesting the antiangiogenic activity of LMWF is hypoxia specific.
Hif1a↓,
VEGF↑,
TumCG↓,
TumVol↓, in mice (needed 300mg/kg/day to actually shrink tumor as opposed to slowing growth)
TumW↓, in mice
Iron∅, maintaining Fe2+ availability through suppression of hypoxia-induced ROS formation is crucial for promoting HIF-1 degradation and diminishing HIF-1 activity by preventing PHD and FIH inactivation
ROS↓, LMWF may target different levels, including inhibition of ROS formation

2825- FIS,    Exploring the molecular targets of dietary flavonoid fisetin in cancer
- Review, Var, NA
*Inflam↓, present in fruits and vegetables such as strawberries, apple, cucumber, persimmon, grape and onion, was shown to possess anti-microbial, anti-inflammatory, anti-oxidant
*antiOx↓, fisetin possesses stronger oxidant inhibitory activity than well-known potent antioxidants like morin and myricetin.
*ERK↑, inducing extracellular signal-regulated kinase1/2 (ERK)/c-myc phosphorylation, nuclear NF-E2-related factor-2 (Nrf2), glutamate cystine ligase and glutathione (GSH) levels
*p‑cMyc↑,
*NRF2↑,
*GSH↑,
*HO-1↑, activate Nrf2 mediated induction of hemeoxygenase-1 (HO-1) important for cell survival
mTOR↓, in our studies on fisetin in non-small lung cancer cells, we found that fisetin acts as a dual inhibitor PI3K/Akt and mTOR pathways
PI3K↓,
Akt↓,
TumCCA↑, fisetin treatment to LNCaP cells resulted in G1-phase arrest accompanied with decrease in cyclins D1, D2 and E and their activating partner CDKs 2, 4 and 6 with induction ofWAF1/p21 and KIP1/p27
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
CDK6↓,
P21↑,
p27↑,
JNK↑, fisetin could inhibit the metastatic ability of PC-3 cells by suppressing of PI3 K/Akt and JNK signaling pathways with subsequent repression of matrix metalloproteinase-2 (MMP-2) and MMP-9
MMP2↓,
MMP9↓,
uPA↓, fisetin suppressed protein and mRNA levels of MMP-2 and urokinase-type plasminogen activator (uPA) in an ERK-dependent fashion.
NF-kB↓, decrease in the nuclear levels of NF-B, c-Fos, and c-Jun was noted in fisetin treated cells
cFos↓,
cJun↓,
E-cadherin↑, upregulation of E-cadherin and down-regulation of vimentin and N-cadherin.
Vim↓,
N-cadherin↓,
EMT↓, EMT inhibiting potential of fisetin has been reported in melanoma cells
MMP↓, The shift in mitochondrial membrane potential was accompanied by release of cytochrome c and Smac/DIABLO resulting in activation of the caspase cascade and cleavage of PARP
Cyt‑c↑,
Diablo↑,
Casp↑,
cl‑PARP↑,
P53↑, fisetin with induction of p53 protein
COX2↓, Fisetin down-regulated COX-2 and reduced the secretion of prostaglandin E2 without affecting COX-1 protein expression.
PGE2↓,
HSP70/HSPA5↓, It was shown that the induction of HSF1 target proteins, such as HSP70, HSP27 and BAG3 were inhibited in HCT-116 cells exposed to heat shock at 43 C for 1 h in the presence of fisetin
HSP27↓,
DNAdam↑, DNA fragmentation, an increase in the number of sub-G1 phase cells, mitochondrial membrane depolarization and activation of caspase-9 and caspase-3.
Casp3↑,
Casp9↑,
ROS↑, This was associated with production of intracellular ROS
AMPK↑, Fisetin induced AMPK signaling
NO↑, fisetin induced cytotoxicity and showed that fisetin induced apoptosis of leukemia cells through generation of NO and elevated Ca2+ activating the caspase
Ca+2↑,
mTORC1↓, Fisetin was shown to inhibit the mTORC1 pathway and its downstream components including p70S6 K, eIF4B and eEF2 K.
p70S6↓,
ROS↓, Others have also noted a similar decrease in ROS with fisetin treatment.
ER Stress↑, Induction of ER stress upon fisetin treatment, evident as early as 6 h, and associated with up-regulation of IRE1, XBP1s, ATF4 and GRP78, was followed by autophagy which was not sustained
IRE1↑,
ATF4↑,
GRP78/BiP↑,
eff↑, Combination of fisetin and the BRAF inhibitor sorafenib was found to be extremely effective in inhibiting the growth of BRAF-mutated human melanoma cells
eff↑, synergistic effect of fisetin and sorafenib was observed in human cervical cancer HeLa cells,
eff↑, Similarly, fisetin in combination with hesperetin induced apoptosis
RadioS↑, pretreatment with fisetin enhanced the radio-sensitivity of p53 mutant HT-29 cancer cells,
ChemoSen↑, potential of fisetin in enhancing cisplatin-induced cytotoxicity in various cancer models
Half-Life↝, intraperitoneal (ip) dose of 223 mg/kg body weight the maximum plasma concentration (2.53 ug/ml) of fisetin was reached at 15 min which started to decline with a first rapid alpha half-life of 0.09 h and a longer half-life of 3.12 h.

2892- HNK,    Honokiol Induces Apoptosis, G1 Arrest, and Autophagy in KRAS Mutant Lung Cancer Cells
- in-vitro, Lung, A549 - in-vitro, Lung, H460 - in-vitro, Lung, H385 - in-vitro, Nor, BEAS-2B
TumCCA↑, Honokiol was shown to induce G1 arrest and apoptosis to inhibit the growth of KRAS mutant lung cancer cells
Apoptosis↑,
SIRT3↑, we also discovered that Sirt3 was significantly up-regulated in honokiol treated KRAS mutant lung cancer cells,
Hif1a↓, leading to destabilization of its target gene Hif-1α, (accompanied by a reduction of Hif-1a expression)
selectivity↑, but it showed low toxicity to two normal lung cells (CCD19-Lu and BEAS-2B)
p‑mTOR↓, honokiol suppressed mTOR phosphorylation, leading to inhibition of P70S6K kinase activity,
p70S6↓,

4212- Hup,    Huperzine A Alleviates Oxidative Glutamate Toxicity in Hippocampal HT22 Cells via Activating BDNF/TrkB-Dependent PI3K/Akt/mTOR Signaling Pathway
- in-vitro, Nor, HT22
*ROS↓, 10 μM HupA for 24 h significantly protected HT22 from cellular damage and suppressed the generation of ROS.
*p‑Akt↓, HupA dramatically prevented the down-regulations of p-Akt, p-mTOR, and p-p70s6 kinase in HT22 cells under oxidative toxicity
*p‑mTOR↓,
*p‑p70S6↓,
*BDNF↑, the protein levels of BDNF and p-TrkB were evidently enhanced after co-treatment with HupA and glutamate in HT22 cells.
*Apoptosis↓, Cellular apoptosis was significantly suppressed (decreased caspase-3 activity and enhanced Bcl-2 protein level) after HupA treatment.
*Casp3↓,
*Bcl-2↑,

971- MEL,    Melatonin down-regulates HIF-1 alpha expression through inhibition of protein translation in prostate cancer cells
- in-vitro, Pca, DU145 - in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP
Hif1a↓, inhibit expression of HIF-1 alpha protein under both normoxic and hypoxic conditions in DU145, PC-3, and LNCaP prostate cancer cells without affecting HIF-1 alpha mRNA levels
VEGF↓,
p‑p70S6↓,

1458- SFN,    Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma
- Review, Bladder, NA
HDAC↓, SFN’s role as a natural HDAC-inhibitor is highly relevant
eff↓, SFN exerts stronger anti-proliferative effects on bladder cancer cell lines under hypoxia, compared to normoxic conditions
TumW↓, mice, SFN (52 mg/kg body weight) for 2 weeks reduced tumor weight by 42%
TumW↓, In another study a 63% inhibition was noted when tumor bearing mice were treated with SFN (12 mg/kg body weight) for 5 weeks
angioG↓,
*toxicity↓, In both investigations, the administration of SFN did not evoke apparent toxicity
GutMicro↝, SFN may protect against chemical-induced bladder cancer by normalizing the composition of gut microbiota and repairing pathophysiological destruction of the gut barrier,
AntiCan↑, A prospective study involving nearly 50,000 men indicated that high cruciferous vegetable consumption may reduce bladder cancer risk
ROS↑, Evidence shows that SFN upregulates the ROS level in T24 bladder cancer cells to induce apoptosis
MMP↓,
Cyt‑c↑,
Bax:Bcl2↑,
Casp3↑,
Casp9↑,
Casp8∅,
cl‑PARP↑,
TRAIL↑, ROS generation promotes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sensitivity
DR5↑,
eff↓, Blockade of ROS generation inhibited apoptotic activity and prevented Nrf2 activation in cells treated with SFN, pointing to a direct effect of ROS on apoptosis
NRF2↑, SFN potently inhibits carcinogenesis via activation of the Nrf2 pathway
ER Stress↑, endoplasmic reticulum stress evoked by SFN
COX2↓, downregulates COX-2 in T24 cells
EGFR↓, downregulation of both the epidermal growth factor receptor (EGFR) and the human epidermal growth factor receptor 2 (HER2/neu
HER2/EBBR2↓,
ChemoSen↑, gemcitabine/cisplatin and SFN triggered pathway alterations in bladder cancer may open new therapeutic strategies, including a combined treatment regimen to cause additive effects.
NF-kB↓,
TumCCA?, cell cycle at the G2/M phase
p‑Akt↓,
p‑mTOR↓,
p70S6↓,
p19↑, p19 and p21, are elevated under SFN
P21↑,
CD44↓, CD44s expression correlates with induced intracellular levels of ROS in bladder cancer cells variants v3–v7 on bladder cancer cells following SFN exposure
CSCs↓, CD44 is not only involved in cytoskeletal changes and cellular motility but also serves as a cancer stem cell (CSC) marker

965- SK,    Shikonin suppresses proliferation and induces cell cycle arrest through the inhibition of hypoxia-inducible factor-1α signaling
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW-620
Hif1a↓, shikonin inhibited HIF-1α protein synthesis without affecting the expression of HIF-1α mRNA or degrading HIF-1α protein
ROS↓, shikonin resulted in a significant decrease of hypoxia-induced ROS production in HCT116 and SW620 cells
mTOR↓,
p70S6↓,
4E-BP1↓,
eIF2α↓,
TumCCA↑, HCT116 cells
TumCP↓, HCT116 and SW620
Half-Life↝, shikonin-treated cells (Fig. S1), showing the half-life was around 50 min in HCT116 and SW620 cells.

4853- Uro,    Urolithin A, a novel natural compound to target PI3K/AKT/mTOR pathway in pancreatic cancer
- vitro+vivo, PC, MIA PaCa-2 - in-vitro, NA, PANC1
p‑Akt↓, treatment of PDAC cells with Uro A blocked the phosphorylation of AKT and p70S6K in vitro, successfully inhibited the growth of tumor xenografts, and increased overall survival (OS)
p‑p70S6↓,
TumCG↓,
OS↑,
PI3K↓, Uro A as a therapeutic agent in PDAC through suppression of the PI3K/AKT/mTOR pathway.
mTOR↓,
TumCP↓, Uro A treatment inhibits PDAC cell proliferation, migration, and enhances apoptosis
TumCMig↓,
Apoptosis↑,
TAMS↓, Improved therapeutic response to Uro A treatment is associated with a reduction in immunosuppressive tumor- associated macrophages (TAMs) and regulatory T cells (Tregs) in PKT mice
Treg lymp↓,
Wnt↓, Uro A is known to mediate its anti-tumor activities through downregulation of Wnt and IGF-1 signaling in colon and prostate cancer cells
IGF-1↓,
*toxicity↓, A Phase I clinical trial of Uro A demonstrated that it is well-tolerated with good bioavailability
*BioAv↑,
Half-Life↝, Uro A is rapidly absorbed and reaches peak plasma concentration two hours after ingestion


Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   Iron∅, 1,   lipid-P↑, 1,   NRF2↑, 1,   ROS↓, 3,   ROS↑, 4,   SIRT3↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 3,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   p‑PDK1↓, 1,   p‑PI3k/Akt/mTOR↓, 1,   p‑PIK3R1↓, 1,   p‑S6↓, 1,  

Cell Death ⓘ

Akt↓, 5,   p‑Akt↓, 4,   Apoptosis↑, 3,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 2,   Casp8∅, 1,   Casp9↑, 2,   Cyt‑c↑, 2,   Diablo↑, 1,   DR5↑, 1,   JNK↑, 1,   p‑JNK↑, 1,   MAPK↑, 1,   p27↑, 1,   p‑p38↑, 1,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,   HER2/EBBR2↓, 1,   p70S6↓, 7,   p‑p70S6↓, 5,   TSC2↑, 2,  

Transcription & Epigenetics ⓘ

cJun↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

eIF2α↓, 1,   eIF2α↑, 1,   ER Stress↑, 3,   GRP78/BiP↑, 2,   HSF1↓, 1,   HSP27↓, 1,   HSP70/HSPA5↓, 1,   HSP70/HSPA5↑, 1,   IRE1↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3II↑, 1,   p62↓, 1,   TumAuto↑, 3,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 1,   cl‑PARP↑, 2,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   p19↑, 1,   P21↑, 2,   TumCCA?, 1,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

4E-BP1↓, 1,   p‑4E-BP1↓, 3,   CD44↓, 1,   cFos↓, 1,   CSCs↓, 1,   EMT↓, 1,   p‑ERK↑, 1,   HDAC↓, 1,   IGF-1↓, 1,   mTOR↓, 5,   p‑mTOR↓, 2,   mTORC1↓, 1,   p85S6K↓, 1,   PI3K↓, 3,   PTEN↑, 1,   TumCG↓, 2,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

Ca+2↑, 1,   E-cadherin↑, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   Treg lymp↓, 1,   TumCMig↓, 1,   TumCP↓, 3,   uPA↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   ATF4↑, 1,   EGFR↓, 1,   Hif1a↓, 4,   NO↑, 1,   TAMS↓, 1,   VEGF↓, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   NF-kB↓, 2,   PGE2↓, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   eff↓, 3,   eff↑, 3,   Half-Life↝, 3,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   GutMicro↝, 1,   HER2/EBBR2↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   OS↑, 1,   TumVol↓, 1,   TumW↓, 3,  
Total Targets: 119

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   GSH↑, 1,   HO-1↑, 1,   NRF2↑, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis ⓘ

p‑cMyc↑, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↓, 1,   Bcl-2↑, 1,   Casp3↓, 1,  

Kinase & Signal Transduction ⓘ

p‑p70S6↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   p‑mTOR↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,  

Functional Outcomes ⓘ

toxicity↓, 2,  
Total Targets: 17

Scientific Paper Hit Count for: p70S6, phospho-S6
1 Apigenin (mainly Parsley)
1 Ashwagandha(Withaferin A)
1 Boron
1 Chrysin
1 Curcumin
1 Fucoidan
1 Fisetin
1 Honokiol
1 Huperzine A/Huperzia serrata
1 Melatonin
1 Sulforaphane (mainly Broccoli)
1 Shikonin
1 Urolithin
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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