STAT3 Cancer Research Results

STAT3, Signal transducer and activator of transcription 3: Click to Expand ⟱
Source:
Type: Oncogene
Stat3 (Signal Transducer and Activator of Transcription 3) is a transcription factor that plays a crucial role in various cellular processes, including cell growth, survival, differentiation, and immune response.
Stat3 is frequently found to be constitutively activated in many types of cancers, including breast, prostate, lung, and head and neck cancers. (associated with poor prognosis and reduced survival.)

-STAT3 is typically activated by cytokines (such as IL-6) and growth factors binding to their respective receptors.
-Activated STAT3 upregulates the expression of genes that promote cell cycle progression (e.g., cyclin D1) and anti-apoptotic proteins (e.g., Bcl-2, Bcl-xL).
Scientific Papers found: Click to Expand⟱
5856- CAP,    Potential of capsaicin as a combinatorial agent to overcome chemoresistance and to improve outcomes of cancer therapy
- Review, Var, NA
ChemoSen↑, has garnered significant interest for its potential role as a combinatorial and chemosensitizing agent in cancer therapy
Apoptosis↑, CAPS enhanced the efficacy of various anticancer agents by promoting apoptosis, modulating autophagy and inhibiting angiogenesis, tumor growth, and metastasis.
TumAuto↑,
angioG↓,
TumCG↓,
TumMeta↓,
P-gp/ABCB1↝, CAPS modulated critical regulators of chemoresistance, such as P-glycoprotein (P-gp), extracellular signal-regulated kinase (ERK), nuclear factor-kappa B (NF-κB) pathway, and signal transducer and activator of transcription 3 (STAT3) pathway
ERK↝,
NF-kB↝,
STAT3↝,
eff↑, combination with chemotherapeutic agents, CAPS has been shown to improve treatment efficacy at lower drug concentrations.

7873- isoO,    Isoorientin attenuates doxorubicin-induced cardiac injury via the activation of MAPK, Akt, and Caspase-dependent signaling pathways
- in-vitro, Liver, HepG2 - in-vitro, CRC, HT-29 - in-vitro, Lung, A549
ChemoSen↑, The antiproliferation of DOX on Hela, HepG2, HT-29, and A549 cells could be increased synergistically when cotreated with ISO in vitro. I
TumCP↓,
chemoP↑, ISO could also improve the survival rate of DOX-injured cardiomyocytes by reducing reactive oxygen species, maintaining mitochondrial function, and inhibiting apoptosis.
*ROS↓,
*mtDam↓,
*Apoptosis↓,
*cardioP↑, In mice receiving DOX, a protective effect on myocardial tissue, which was reflected by improved survival state of mice receiving chemotherapy, was observed.
*NRF2↑, ISO upregulated Nrf2 and TGF-β3 by downregulating the phosphorylation levels of JNK and p38 proteins on the MAPK pathway and the Akt and Stat3 expression levels.
*TGF-β↑,
*p‑JNK↓,
*p‑p38↓,
*MAPK↝,
*Akt↝,
*STAT3↝,

8040- IVM,    Ivermectin, a potential anticancer drug derived from an antiparasitic drug
- Review, Var, NA
Akt↓, inhibition by IVM of the Akt/mTOR pathway to induce autophagy and p-21-activated kinase 1(PAK1)was the target of IVM for breast cancer
mTOR↓,
TumAuto↑,
TumCP↓, IVM could inhibit the proliferation of the canine breast tumor cell lines CMT7364 and CIPp by blocking the cell cycle without increasing apoptosis, and the mechanism of IVM may be related to the inhibition of the Wnt pathway
TumCCA↑,
Wnt↓,
YAP/TEAD↓,
MMP↓, IVM could significantly reduce the mitochondrial membrane potential and inhibit mitochondrial respiration and ATP production.
mitResp↓,
ATP↓,
eff↓, acetyl-L-cysteine (NAC), could reverse IVM-induced inhibition
eff↑, it was found that IVM could enhance the drug activity of the anti-androgen drug enzalutamide in the prostate cancer cell line LNCaP and reverse the resistance of the prostate cancer cell line PC3 to docetaxel
ROS↑, induction of reactive oxygen species (ROS) production.
ChemoSen↑, IVM can enhance the efficacy of cisplatin to improve the treatment of epithelial ovarian cancer, and the mechanism is related to the inhibition of the Akt/mTOR pathway
PAK1↓, IVM also had a cytotoxic effect on a variety of nasopharyngeal cancer cells in vitro, and the mechanism is related to the reduction of PAK1 kinase activity to inhibit the MAPK pathway.
MAPK↓,
EMT↓, IVM could reduce the metastasis of lung cancer cells by inhibiting EMT.
Beclin-1/ATG6↑, IVM in the breast cancer cell lines MCF-7 and MDA-MB-231 significantly increased intracellular autophagic flux and the expression of key autophagy proteins such as LC3, Bclin1, Atg5
ATG5↑,
CSCs↓, Further studies showed that IVM could inhibit CSCs by regulating the PAK1-STAT3 axis
STAT3↝,
P-gp/ABCB1↓, Several studies have confirmed that IVM could reverse drug resistance by inhibiting P-gp and MDR-associated proteins
MDR1↓,
HSP27↓, Inhibit HSP27 Prostate cancer, Lung cancer Colorectal cancer
Chl↑, Activate chloride channels Leukemia
TFE3↑, Increase TFE3 Activity Melanoma

4649- OLEC,    Anticancer molecular mechanisms of oleocanthal
Apoptosis↑, the major mechanisms of action of OLC include modulation of the apoptotic pathway, the HGF/c-Met pathway, and the signal transducer and activator of transcription 3 signaling pathway, among others.
HGF/c-Met↝,
STAT3↝,


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

TFE3↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   mitResp↓, 1,   MMP↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 2,   HGF/c-Met↝, 1,   MAPK↓, 1,   YAP/TEAD↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP27↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 1,   TumAuto↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

CSCs↓, 1,   EMT↓, 1,   ERK↝, 1,   mTOR↓, 1,   STAT3↝, 3,   TumCG↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

Chl↑, 1,   PAK1↓, 1,   TumCP↓, 2,   TumMeta↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,   P-gp/ABCB1↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

NF-kB↝, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 3,   eff↓, 1,   eff↑, 2,   MDR1↓, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1,  
Total Targets: 35

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

NRF2↑, 1,   ROS↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

mtDam↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↝, 1,   Apoptosis↓, 1,   p‑JNK↓, 1,   MAPK↝, 1,   p‑p38↓, 1,  

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

STAT3↝, 1,  

Migration(tgid=13) ⓘ

TGF-β↑, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,  
Total Targets: 11

Scientific Paper Hit Count for: STAT3, Signal transducer and activator of transcription 3
1 Capsaicin
1 isoorientin
1 Ivermectin
1 Oleocanthal
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#:373  State#:%  Dir#:4
  wNotes=on  sortOrder:rid,rpid

 

Home Page