P70S6K Cancer Research Results

P70S6K, p70 S6 kinase: Click to Expand ⟱

Source:

Type:

P70S6K, or p70 S6 kinase, is a protein kinase that plays a significant role in the signaling pathways related to cell growth, proliferation, and survival. It is part of the mTOR (mechanistic target of rapamycin) signaling pathway, which is crucial for regulating cellular metabolism and growth in response to nutrients, growth factors, and stress signals.

Expression Direction:
In many cancers, p70S6K is frequently found to be overexpressed or hyperactivated. Increased phosphorylation (activation) of p70S6K is often detected, correlating with enhanced mTOR signaling.

Elevated levels or hyperactivation of p70S6K in tumor tissues are generally associated with: More aggressive tumor behavior and higher proliferative indices.
A poorer prognosis in several cancer types.
• In cancers such as breast, lung, and gastrointestinal cancers, high p70S6K activity may correlate with advanced disease and decreased overall survival.

Scientific Papers found: Click to Expand⟱

3434-

ALA,

Alpha lipoic acid modulates metabolic reprogramming in breast cancer stem cells enriched 3D spheroids by targeting phosphoinositide 3-kinase: In silico and in vitro insights

in-vitro,

BC,

MCF-7

in-vitro,

BC,

MDA-MB-231

tumCV↓, significant dose-dependent reduction in cell viability, with the half-maximal inhibitory concentration (IC50) of LA to be 3.2 mM for MCF-7 cells and 2.9 mM for MDA-MB-231 cells
PI3K↓, LA significantly inhibited PI3K, p-AKT, p-p70S6K and p-mTOR levels
p‑Akt↓,
p‑P70S6K↓,
mTOR↓,
ATP↓, LA markedly reduced both ATP levels and glucose uptake (Fig. 4A and 4B). LA also induced ROS generation in both MCF-7 and MDA-MB231 spheroids
GlucoseCon↓,
ROS↑,
PKM2↓, LA downregulated the expression of PKM2 and LDHA in the spheroids, indicating an inhibition of glycolysis in BCSCs
LDHA↓,
Glycolysis↓,
ChemoSen↑, LA enhances chemosensitivity of spheroids to Dox treatment

1545-

Api,

The Potential Role of Apigenin in Cancer Prevention and Treatment

Review,

NA,

TNF-α↓, Apigenin downregulates the TNFα
IL6↓,
IL1α↓,
P53↑,
Bcl-xL↓,
Bcl-2↓,
BAX↑,
Hif1a↓, Apigenin inhibited HIF-1alpha and vascular endothelial growth factor expression
VEGF↓,
TumCCA↑, Apigenin exposure induces G2/M phase cell cycle arrest, DNA damage, apoptosis and p53 accumulation
DNAdam↑,
Apoptosis↑,
CycB/CCNB1↓,
cycA1/CCNA1↓,
CDK1↓,
PI3K↓,
Akt↓,
mTOR↓,
IKKα↓, , decreases IKKα kinase activity,
ERK↓,
p‑Akt↓,
p‑P70S6K↓,
p‑S6↓,
p‑ERK↓, decreased the expression of phosphorylated (p)-ERK1/2 proteins, p-AKT and p-mTOR
p‑P90RSK↑,
STAT3↓,
MMP2↓, Apigenin down-regulated Signal transducer and activator of transcription 3target genes MMP-2, MMP-9 and vascular endothelial growth factor
MMP9↓,
TumCP↓, Apigenin significantly suppressed colorectal cancer cell proliferation, migration, invasion and organoid growth through inhibiting the Wnt/β-catenin signaling
TumCMig↓,
TumCI↓,
Wnt/(β-catenin)↓,

2696-

BBR,

Berberine regulates proliferation, collagen synthesis and cytokine secretion of cardiac fibroblasts via AMPK-mTOR-p70S6K signaling pathway

in-vivo,

Nor,

 1-3 day-old SD rats

*α-SMA↓, It was demonstrated that treatment of cardiac fibroblasts with berberine resulted in deceased proliferation, and attenuated fibroblast α-smooth muscle actin expression and collagen synthesis.
*TGF-β1↓, protein secretion of TGFβ1 was inhibited; however, the protein secretion of IL-10 was increased in cardiac fibroblasts with berberine treatment.
*IL10↑,
*p‑AMPK↑, Mechanistically, the phosphorylation level of AMPK was increased
*p‑mTOR↓, phosphorylation levels of mTOR and p70S6K were decreased in berberine treatment group
*P70S6K↓,
*cardioP↑, protective effects of berberine on cellular behaviors of cardiac fibroblasts

3680-

BBR,

Network pharmacology reveals that Berberine may function against Alzheimer’s disease via the AKT signaling pathway

in-vivo,

AD,

3 × Tg AD mice

*Akt↑, Akt1 mRNA expression levels were significantly decreased in AD mice and significantly increased after BBR treatment (p < 0.05).
*neuroP↑, BBR may exert a neuroprotective effect by modulating the ERK and AKT signaling pathways.
*p‑ERK↑, Besides, AKT and ERK phosphorylation decreased in the model group, and BBR significantly increased their phosphorylation levels.
*Aβ↓, BBR has therapeutic potential in the treatment of AD by targeting amyloid beta plaques, neurofibrillary tangles, neuroinflammation, and oxidative stress
*Inflam↓,
*ROS↓,
*BioAv↑, oral bioavailability (OB) = 36.86%, drug-likeness (DL) = 0.78,
*BBB↑, blood brain barrier (BBB) = 0.57,
*Half-Life↝, half-life (HL) = 6.57. BBR half-life (t1/2) is in the mid-elimination group.
*memory↑, BBR improves the performance of memory and recognition tasks in AD mice
*cognitive↑,
*HSP90↑, Among the core targets, Akt1 (t = −5.01, p = 0.002), Hsp90aa1 (t = −3.66, p = 0.011), Hras (t = −2.99, p = 0.024) and Igf1 (t = 3.75, p = 0.019) mRNA levels were significantly increased after BBR treatment
*APP↓, BBR reduces Aβ levels by modulating APP processing and ameliorates Aβ pathology by inhibiting the mTOR/p70S6K signaling pathway
*mTOR↓,
*P70S6K↓,
*CD31↑, it promotes the formation of brain microvessels by enhancing CD31, VEGF, N-cadherin, Ang-1 and inhibits neuronal apoptosis (Ye et al., 2021).
*VEGF↑,
*N-cadherin↑,
*Apoptosis↓,

5729-

BF,

Bufalin: a potential drug for regulating EGFR-TKIs resistance in lung cancer via the EGFR-PI3K/Akt-mTOR signaling

in-vitro,

Lung,

TumCCA↑, Bufalin and gefitinib could control the cell cycle, induce apoptosis, and impede H1975 cell development and growth.
Apoptosis↑,
TumCG↓,
EGFR↓, bufalin and gefitinib inhibited the growth of lung cancer tumor and decreased the expression of proteins pertinent to the EGFR-PI3K/Akt-mTOR pathway, including EGFR, Akt, mTOR, and p70S6K.
PI3K↓,
Akt↓,
mTOR↓,
P70S6K↓,

5940-

Cela,

Celastrol Suppresses Angiogenesis-Mediated Tumor Growth through Inhibition of AKT/Mammalian Target of Rapamycin Pathway

in-vivo,

Pca,

PC3

mice

Dose↝, When administered subcutaneously to mice bearing human prostate cancer (PC-3 cell) xenografts, Celastrol (2 mg/kg/d)
TumVol↓, significantly reduced the volume and the weight of solid tumors and decreased tumor angiogenesis.
TumW↓,
angioG↓,
VEGF↓, this agent inhibited vascular endothelial growth factor (VEGF)-induced proliferation, migration, invasion,
TumCMig↓,
TumCP↓,
TumCI↓,
Akt↓, Celastrol suppressed the VEGF-induced activation of AKT, mammalian target of rapamycin (mTOR), and ribosomal protein S6 kinase (P70S6K)
mTOR↓,
P70S6K↓,

471-

CUR,

Curcumin induces apoptotic cell death and protective autophagy by inhibiting AKT/mTOR/p70S6K pathway in human ovarian cancer cells

in-vitro,

Ovarian,

SKOV3

5, 10, 20, 40 and 80 μM, 24, 48 and 72 h

in-vitro,

Ovarian,

A2780S

Apoptosis↑,
TumAuto↑,
p62↓,
p‑Akt↓,
p‑mTOR↓,
p‑P70S6K↓,
Casp9↑,
PARP↑,
ATG3↑,
Beclin-1↑,
LC3‑Ⅱ/LC3‑Ⅰ↑,

972-

MAG,

Magnolol suppresses hypoxia-induced angiogenesis via inhibition of HIF-1α/VEGF signaling pathway in human bladder cancer cells

vitro+vivo,

Bladder,

T24/HTB-9

angioG↓,
VEGF↓,
H2O2↓,
Hif1a↓,
VEGFR2↓,
Akt↓,
mTOR↓,
P70S6K↓,
4E-BP1↓,
TumCG↓,
CD31↓,
CA↓, carbonic anhydrase IX

2376-

MET,

Metformin Inhibits Epithelial-to-Mesenchymal Transition of Keloid Fibroblasts via the HIF-1α/PKM2 Signaling Pathway

in-vitro,

Nor,

10, 15, 20 mM

*Hif1a↓, Metformin significantly inhibited the expression of HIF-1α and partially abolished hypoxia-induced EMT.
*EMT↓,
*p‑P70S6K↓, PKM2 is involved in hypoxia-induced EMT of KFs and metformin decreased the expression of p-p70s6k and PKM2.
*PKM2↓, Metformin reverses EMT in keloids through inhibition of the HIF-1α/PKM2 pathway

2377-

MET,

Metformin Inhibits TGF-β1-Induced Epithelial-to-Mesenchymal Transition via PKM2 Relative-mTOR/p70s6k Signaling Pathway in Cervical Carcinoma Cells

in-vitro,

Cerv,

HeLa

in-vitro,

Cerv,

SiHa

EMT↓, metformin partially abolished TGF-β1-induced EMT cell proliferation
P70S6K↓, Metformin decreased the p-p70s6k expression and the blockade of mTOR/p70s6k signaling decreased PKM2 expression.
mTOR↓,
PKM2↓,
Warburg↓, PKM2 regulates in the cancer-specific Warburg effect, which is responsible for the final rate-limiting step of glycolysis.
AMPK↑, direct mechanisms involving activating AMP-activated protein kinase (AMPK), followed by inhibition of the mammalian target of the rapamycin (mTOR) pathway

2386-

MET,

Mechanisms of metformin inhibiting cancer invasion and migration

Review,

Var,

OS↑, Also, in Canada, a large retrospective study was conducted, and the results indicated a 20% reduction of cancer-specific mortality among metformin users compared to its non-users
AMPK↑, Metformin inhibits invasion and migration through the AMPK signaling pathway
EMT↓, Metformin inhibits invasion and migration through EMT signaling pathways
TGF-β↓, The invasive ability of pancreatic cancer cells is suppressed by metformin by blocking signaling in the autocrine TGF-β1 pathway
mTOR↓, Furthermore, TGF-β1-induced EMT in cervical carcinoma cells is abolished by metformin through inhibiting the mTOR/p70s6k signaling pathway to down-regulate PKM2 expression
P70S6K↓,
PKM2↓,
Hif1a↓, Subsequently, it was discovered that gastric cancer was inhibited by metformin via the inhibition of HIF1α/PKM2 signaling
ChemoSen↑, it increased the sensitivity of chemotherapy drugs to different types of cancer

1664-

PBG,

Anticancer Activity of Propolis and Its Compounds

Review,

Var,

Apoptosis↑,
TumCMig↓,
TumCCA↑,
TumCP↓,
angioG↓,
P21↑, upregulating p21 and p27 expression
p27↑,
CDK1↓, thanol-extracted Cameroonian propolis increased the amount of DU145 and PC3 cells in G0/G1 phase, down-regulated cell cycle proteins (CDK1, pCDK1, and their related cyclins A and B)
p‑CDK1↓,
cycA1/CCNA1↓,
CycB/CCNB1↓,
P70S6K↓, Caffeic acid phenylethyl ester has been shown to inhibit the S6 beta-1 ribosomal protein kinase (p70S6K),
CLDN2↓, inhibition of NF-κB may be involved in the decrease of claudin-2 mRNA level
HK2↓, Chinese poplar propolis has been shown to significantly reduce the level of glycolysis at the stage of action of hexokinase 2 (HK2), phosphofructokinase (PFK), muscle isozyme pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA)
PFK↓,
PKM2↓,
LDHA↓,
TLR4↓, hinese propolis, as well as CAPE, inhibits breast cancer cell proliferation in the inflammatory microenvironment by inhibiting the Toll-like receptor 4 (TLR4) signal pathway
H3↓, Brazilian red propolis bioactive isoflavonoid, down-regulates the alpha-tubulin, tubulin in microtubules, and histone H3 genes
α-tubulin↓,
ROS↑, CAPE also affects the apoptotic intrinsic pathway by increasing ROS production
Akt↓, CAPE induces apoptosis by decreasing the levels of proteins related to carcinogenesis, including Akt, GSK3b, FOXO1, FOXO3a, NF-kB, Skp2 and cyclin D1
GSK‐3β↓,
FOXO3↓,
NF-kB↓,
cycD1/CCND1↓,
MMP↓, It was found that chrysin caused a loss of mitochondria membrane potential (MMP) while increasing the production of reactive oxygen species (ROS), cytoplasmic Ca2+ levels, and lipid peroxidation
ROS↑,
i-Ca+2↑,
lipid-P↑,
ER Stress↑, Chrysin also induced endoplasmic reticulum (ER) stress by activating unfolded protein response proteins (UPR) such as PRKR-like ER kinase (PERK), eukaryotic translation initiation factor 2α (eIF2α), and 78 kDa glucose-regulated protein (GRP78)
UPR↑,
PERK↑,
eIF2α↑,
GRP78/BiP↑,
BAX↑, CAPE activated Bax protein
PUMA↑, CAPE also significantly increased PUMA expression
ROS↑, Northeast China causes cell apoptosis in human gastric cancer cells with increased production of reactive oxygen species (ROS) and reduced mitochondrial membrane potential.
MMP↓,
Cyt‑c↑, release of cytochrome C from mitochondria to the cytoplasm is observed, as well as the activation of cleaved caspases (8, 9, and 3) and PARP
cl‑Casp8↑,
cl‑Casp8↑,
cl‑Casp3↑,
cl‑PARP↑,
eff↑, administration of Iranian propolis extract in combination with 5-fluorouracil (5-FU) significantly reduced the number of azaxymethane-induced aberrant crypt foci compared to 5-FU or propolis alone.
eff↑, Propolis may also have a positive effect on the efficacy of photodynamic therapy (PDT). enhances the intracellular accumulation of protoporphyrin IX (PpIX) in human epidermoid carcinoma cells
RadioS↑, breast cancer patients undergoing radiotherapy and supplemented with propolis had a statistically significant longer median disease-free survival time than the control group
ChemoSen↑, confirmed that propolis mouthwash is effective and safe in the treatment of chemo- or radiotherapy-induced oral mucositis in cancer patients.
eff↑, Quercetin, ferulic acid, and CAPE may also influence the MDR of cancer cells by inhibiting P-gp expression

4704-

PTS,

Cisplatin,

Pterostilbene Sensitizes Cisplatin-Resistant Human Bladder Cancer Cells with Oncogenic HRAS

in-vitro,

Bladder,

PI3K↓, Pterostilbene-induced autophagy in T24 cells was paralleled by inhibition of class I PI3K/mTOR/p70S6K as well as activation of MEK/ERK (a RAS target) and class III PI3K pathways.
mTOR↓,
P70S6K↓,
MEK↑,
ERK↑,
ChemoSen↑, Animal study data confirmed that pterostilbene enhanced cytotoxicity of cisplatin plus gemcitabine.
TumAuto↑, Pterostilbene-Enhanced Cytotoxic Response to Food and Drug Administration (FDA)-Approved Anticancer Drugs Was Indeed Associated with an Induction of Autophagy

39-

QC,

A Comprehensive Analysis and Anti-Cancer Activities of Quercetin in ROS-Mediated Cancer and Cancer Stem Cells

Analysis,

NA,

ROS↑, production of ROS in both cancer, and cancer stem cells,
GSH↓, By directly reducing the intracellular pool of glutathione (GSH), QC can influence ROS metabolism
IL6↓, QC is its ability to inhibit inflammatory mediators including IFN-γ, IL-6, COX-2, IL-8, iNOS, TNF-α, and many other cancer inflammatory mechanisms
COX2↓,
IL8↓,
iNOS↓,
TNF-α↓,
MAPK↑, quercetin-3-methyl ether stopped the growth of cancer in the esophagus by blocking the Akt/mTOR/P70S6k and MAPK pathways, which are important for the growth of cancer
ERK↑,
SOD↑,
ATP↓,
Casp↑,
PI3K/Akt↓,
mTOR↓,
NOTCH1↓,
Bcl-2↓,
BAX↑,
IFN-γ↓,
TumCP↓, QC directly involves inducing apoptosis and/or the cell cycle arrest process, and also inhibits the propagation of rapidly proliferating cells
TumCCA↑,
Akt↓, quercetin-3-methyl ether stopped the growth of cancer in the esophagus by blocking the Akt/mTOR/P70S6k and MAPK pathways, which are important for the growth of cancer
P70S6K↓,
*Keap1↓,
*GPx↑, inhibiting its negative regulator, Keap1, resulting in Nrf-2 nuclear translocation [86]. This results in the production and activation of enzymes namely GPX, CAT, heme oxygenase 1 (HO-1), peroxiredoxin (PRX)
*Catalase↑,
*HO-1↑,
*NRF2↑,
NRF2↑, The effect of QC on nuclear translocation of Nrf-2 in a time-dependent manner, and increased expression level in HepG2, MgM (malignant mesothelioma) MSTO-211H, and H2452 cells at mRNA and protein quantity has been reported recently
eff↑, quercetin coupled with gold nanoparticles promoted apoptosis by inhibiting the EGFR/P13K/Akt-mediated pathway
HIF-1↓, Quercetin has been shown to suppress the Akt-mTOR pathway and hypoxia-induced factor 1 signaling pathway in gastric cancer cells, resulting in preventative autophagy

92-

QC,

Quercetin Inhibits Angiogenesis Mediated Human Prostate Tumor Growth by Targeting VEGFR- 2 Regulated AKT/mTOR/P70S6K Signaling Pathways

vitro+vivo,

Pca,

HUVECs

 10, 20, 30, 40 umol/L;

vitro+vivo,

Pca,

PC3

 20mg/kg/day

VEGFR2↓, Quercetin treatment inhibited the activation of VEGF-R2 and thereby suppressed the AKT/mTOR/P70S6K mediated angiogenesis signaling pathways.
HemoG↓,
Akt↓, AKT/mTOR/P70S6K↓
mTOR↓,
P70S6K↓,
angioG↓, quercetin is a potent inhibitor of angiogenesis in vitro, ex vivo and in vivo.

3002-

RosA,

Anticancer Effects of Rosemary (Rosmarinus officinalis L.) Extract and Rosemary Extract Polyphenols

Review,

Var,

TumCG↓, SW480 colon cancer cells and found RE to significantly decrease cell growth at a concentration of 31.25 µg/mL (48 h),
TumCP↓, Cell proliferation was dramatically decreased and cell cycle arrest was induced in HT-29 and SW480 c
TumCCA↑,
ChemoSen↑, RE enhanced the inhibitory effects of the chemotherapeutic drug 5-fluorouracil (5-FU) on proliferation and sensitized 5-FU resistant cells
NRF2↑, HCT116 ↑ Nrf2, ↑ PERK, ↑ sestrin-2, ↑ HO-1, ↑ cleaved-casp 3
PERK↑,
SESN2↑,
HO-1↑,
cl‑Casp3↑,
ROS↑, HT-29 ↑ ROS accumulation, ↑ UPR, ↑ ER-stress
UPR↑,
ER Stress↑,
CHOP↑, HT-29: ↑ ROS levels, ↑ HO-1 and CHOP
HER2/EBBR2↓, SK-BR-3: ↑ FOS levels, ↑ PARP cleavage, ↓ HER2, ↓ ERBB2, ↓ ERα receptor.
ER-α36↓,
PSA↓, LNCaP : ↑ CHOP, ↓ PSA production, ↑ Bax, ↑ cleaved-casp 3, ↓ androgen receptor expression
BAX↑,
AR↓,
P-gp↓, A2780: ↓ P-glyco protein, ↑ cytochrome c gene, ↑ hsp70 gene
Cyt‑c↑,
HSP70/HSPA5↑,
eff↑, This study noted that the rosemary essential oil was more potent than its individual components (α-pinene, β-pinene, 1,8-cineole) when tested alone at the same concentrations.
p‑Akt↓, A549: ↓ p-Akt, ↓ p-mTOR, ↓ p-P70S6K, ↑ PARP cleavage
p‑mTOR↓,
p‑P70S6K↓,
cl‑PARP↑,
eff↑, RE containing 10 µM equivalent of CA, or 10 µM CA alone (96 h) potentiated the ability of vitamin D derivatives to inhibit cell viability and proliferation, induce apoptosis and cell cycle arrest and increase differentiation of WEHI-3BD murine leukem

3186-

SFN,

A pharmacological inhibitor of NLRP3 inflammasome prevents non-alcoholic fatty liver disease in a mouse model induced by high fat diet

in-vivo,

Nor,

30 mg/kg/day

mice

*NLRP3↓, suppression of NLRP3 inflammasome activation in the liver by SFN as evidenced by decrease in mRNA levels of ASC and caspase-1, caspase-1 enzyme activity, and IL-1β levels.
*ASC↓,
*Casp1↓,
*IL1β↓,
*ALAT↓, SFN treatment resulted in a reduction of the serum levels of ALT and AST increased by HFD
*AST↓,
*AMPK↑, Sulforaphane induces activation of the AMPK-autophagy axis in mouse primary hepatocytes
*mTOR↓, SFN reduced the phosphorylation of mTOR(Ser2448) in primary mouse hepatocytes (Fig. 4D), suggesting that SFN inhibited mTOR activation
*P70S6K↓, SFN suppression of mTOR activation was confirmed by a decrease in p70S6K1 phosphorylation, which is a downstream substrate of mTOR

3289-

SIL,

Silymarin: a promising modulator of apoptosis and survival signaling in cancer

Review,

Var,

*BioAv↝, silymarin’s poor bioavailability and limited thérapeutic efficacy have been overcome by encapsulation of silymarin into nanoparticles
*BioAv↓, Silymarin is barely 20–50% absorbed by the GIT cells and has an absolute oral bioavailability of 0.95%
Fas↑, silibinin, enhances the Fas pathway in most cancers cells by upregulating the Fas and Fas L
FasL↑,
FADD↑, silymarin triggered apoptosis via upregulating the expression of FADD (Fig. 2b), a downstream component of the death receptor pathway, subsequently leading to the cleavage of procaspase 8 and initiation of apoptotic cell death
pro‑Casp8↑,
Apoptosis↑,
DR5↑, silymarin promotes apoptosis through the death receptor-mediated pathway, contributing to its anticancer effects
Bcl-2↑, Bcl-2, an anti-apoptotic protein, was decreased
BAX↑, Bax is also upregulated and leads to the activation of caspase-3.
Casp3↑,
PI3K↓, Silibinin inhibits the PI3K activity, leading to the reduction of FoxM1 (Forkhead box M1) and the subsequent activation of the mitochondrial apoptotic pathway
FOXM1↓,
p‑mTOR↓, inhibiting phosphorylation of several key components in this pathway, such as mTOR, p70S6K and 4E-BP1
p‑P70S6K↓,
Hif1a↓, mTOR pathway signaling in turn may result in low levels of HIF-1α due to the unfavorable conditions of hypoxia.
Akt↑, silibinin activates the Akt pathway in cervical cancer cells. This activation of Akt could have some bearing on the overall antitumor activity of silibinin in cervical cancer cells.
angioG↓, silibinin inhibited STAT3, HIF-1α, and NF-κB, thereby reducing the population of lung macrophages and limiting angiogenesis
STAT3↓,
NF-kB↓,
lipid-P↓, silibinin delays the progression of endometrial carcinoma via inhibiting STAT3 activation and lowering lipid accumulation, which is regulated by SREBP1
eff↑, Sorafenib and silibinin work together to target both liver cancer cells and cancer stem cells. This combination operates by suppressing the STAT3/ERK/AKT pathways and decreasing the production of Mcl-1 and Bcl-2 proteins
CDK1↓, reducing the expression of CDK1, survivin, Bcl-xL, cyclinB1 and Mcl- 1 and simultaneously activate caspases 3 and 9
survivin↓,
CycB/CCNB1↓,
Mcl-1↓,
Casp9↑,
AP-1↓, hindered the activation of transcription factors NF-κB and AP-1
BioAv↑, Liang et al., created a chitosan-based lipid polymer hybrid nanoparticles that boosted the bioavailability of silymarin by 14.38-fold

5103-

SK,

Attenuation of PI3K-Akt-mTOR Pathway to Reduce Cancer Stemness on Chemoresistant Lung Cancer Cells by Shikonin and Synergy with BEZ235 Inhibitor

in-vitro,

NSCLC,

A549

CSCs↓, we found that low doses of shikonin inhibit the proliferation of lung cancer stem-like cells by inhibiting spheroid formation
TumCP↓,
Nanog↓, mRNA level and protein of stemness genes (Nanog and Oct4) were repressed significantly on both sublines.
OCT4↓,
p‑Akt↓, Shikonin reduces the phosphorylated Akt and p70s6k levels, indicating that the PI3K/Akt/mTOR signaling pathway is downregulated by shikonin.
P70S6K↓,
PI3K↓,
mTOR↓,
eff↑, low doses shikonin and dual PI3K-mTOR inhibitor (BEZ235) have a synergistic effect that inhibits the spheroid formation from chemoresistant lung cancer sublines

3427-

TQ,

Chemopreventive and Anticancer Effects of Thymoquinone: Cellular and Molecular Targets

ROS⇅, It appears that the cellular and/or physiological context(s) determines whether TQ acts as a pro-oxidant or an anti-ox- idant in vivo
Fas↑, Figure 2, cell death
DR5↑,
TRAIL↑,
Casp3↑,
Casp8↑,
Casp9↑,
P53↑,
mTOR↓,
Bcl-2↓,
BID↓,
CXCR4↓,
JNK↑,
p38↑,
MAPK↑,
LC3II↑,
ATG7↑,
Beclin-1↑,
AMPK↑,
PPARγ↑, cell survival
eIF2α↓,
P70S6K↓,
VEGF↓,
ERK↓,
NF-kB↓,
XIAP↓,
survivin↓,
p65↓,
DLC1↑, epigenetic
FOXO↑,
TET2↑,
CYP1B1↑,
UHRF1↓,
DNMT1↓,
HDAC1↓,
IL2↑, inflammation
IL1↓,
IL6↓,
IL10↓,
IL12↓,
TNF-α↓,
iNOS↓,
COX2↓,
5LO↓,
AP-1↓,
PI3K↓, invastion
Akt↓,
cMET↓,
VEGFR2↓,
CXCL1↓,
ITGA5↓,
Wnt↓,
β-catenin/ZEB1↓,
GSK‐3β↓,
Myc↓,
cycD1/CCND1↓,
N-cadherin↓,
Snail↓,
Slug↓,
Vim↓,
Twist↓,
Zeb1↓,
MMP2↓,
MMP7↓,
MMP9↓,
JAK2↓, cell proliferiation
STAT3↓,
NOTCH↓,
cycA1/CCNA1↓,
CDK2↓,
CDK4↓,
CDK6↓,
CDC2↓,
CDC25↓,
Mcl-1↓,
E2Fs↓,
p16↑,
p27↑,
P21↑,
ChemoSen↑, Such chemo-potentiating effects of TQ in different cancer cells have been observed with 5-fluorouracil in gastric cancer and colorectal cancer models

Showing Research Papers: 1 to 20 of 20

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 20

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

OS↑, 1, TumVol↓, 1, TumW↓, 1,
Total Targets: 188

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Catalase↑, 1, GPx↑, 1, HO-1↑, 1, Keap1↓, 1, NRF2↑, 1, ROS↓, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, AMPK↑, 1, p‑AMPK↑, 1, PKM2↓, 1,

Cell Death ⓘ

Akt↑, 1, Apoptosis↓, 1, Casp1↓, 1,

Protein Folding & ER Stress ⓘ

HSP90↑, 1,

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1, p‑ERK↑, 1, mTOR↓, 2, p‑mTOR↓, 1, P70S6K↓, 3, p‑P70S6K↓, 1,

Migration ⓘ

APP↓, 1, CD31↑, 1, N-cadherin↑, 1, TGF-β1↓, 1, α-SMA↓, 1,

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1, VEGF↑, 1,

Barriers & Transport ⓘ

BBB↑, 1,

Immune & Inflammatory Signaling ⓘ

ASC↓, 1, IL10↑, 1, IL1β↓, 1, Inflam↓, 1,

Protein Aggregation ⓘ

Aβ↓, 1, NLRP3↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 1, BioAv↝, 1, Half-Life↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 1, AST↓, 1,

Functional Outcomes ⓘ

cardioP↑, 1, cognitive↑, 1, memory↑, 1, neuroP↑, 1,
Total Targets: 44

Scientific Paper Hit Count for: P70S6K, p70 S6 kinase

3 Metformin
2 Berberine
2 Quercetin
1 Alpha-Lipoic-Acid
1 Apigenin (mainly Parsley)
1 Bufalin/Huachansu
1 Celastrol
1 Curcumin
1 Magnolol
1 Propolis -bee glue
1 Pterostilbene
1 Cisplatin
1 Rosmarinic acid
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Shikonin
1 Thymoquinone

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#:488  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

P70S6K Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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