STAT5 Cancer Research Results

STAT5, Signal transducer and activator of transcription 5: Click to Expand ⟱
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Signal Transducer and Activator of Transcription 5 (STAT5) is a transcription factor that plays a crucial role in various cellular processes, including cell growth, differentiation, and survival.
STAT5 can function as an oncogene in certain types of cancer. Its persistent activation has been associated with the development and progression of various malignancies, including breast cancer, prostate cancer, and hematological cancers like leukemia and lymphoma.
High STAT5 expression has been associated with poor prognosis and increased metastasis.
Scientific Papers found: Click to Expand⟱
573- ART/DHA,    Artesunate suppresses tumor growth and induces apoptosis through the modulation of multiple oncogenic cascades in a chronic myeloid leukemia xenograft mouse model
- vitro+vivo, NA, NA
p‑p38↓,
p‑ERK↓,
p‑CREB↓,
p‑Chk2↓,
p‑STAT5↓,
p‑RSK↓,
SOCS1↑,
Apoptosis↑,
Casp3↑,

6184- Cuc,    Cucurbitacin B induces apoptosis by inhibition of the JAK/STAT pathway and potentiates antiproliferative effects of gemcitabine on pancreatic cancer cells
- vitro+vivo, PC, NA
TumCG↓, cucurbitacin B was tested in vitro and in vivo against human pancreatic cancer cells. Dose-response studies showed that the drug inhibited 50% growth of seven pancreatic cancer cell lines at 10(-7) mol/L,
TumCCA↑, Cucurbitacin B caused dose- and time-dependent G(2)-M-phase arrest and apoptosis of pancreatic cancer cells.
Apoptosis↑,
JAK2↓, associated with inhibition of activated JAK2, STAT3, and STAT5, increased level of p21(WAF1) even in cells with nonfunctional p53, and decrease of expression of cyclin A, cyclin B1, and Bcl-XL with subsequent activation of the caspase cascade.
STAT3↓,
STAT5↓,
P21↑,
cycA1/CCNA1↓,
CycB/CCNB1↓,
Bcl-xL↓,
ChemoSen↑, combination of cucurbitacin B and gemcitabine synergistically potentiated the antiproliferative effects of gemcitabine on pancreatic cancer cells.
TumVol↓, cucurbitacin B decreased the volume of pancreatic tumor xenografts in athymic nude mice by 69.2%
toxicity↓, without noticeable drug toxicities.

13- CUR,    Role of curcumin in regulating p53 in breast cancer: an overview of the mechanism of action
- Review, BC, NA
P53↑, upregulated other targets including p53, death receptor (DR-5), JN-kinase, Nrf-2, and peroxisome proliferator-activated receptor γ (PPARγ) factors
DR5↑,
JNK↑,
NRF2↑,
PPARγ↑,
HER2/EBBR2↓, (Her-2, IR, ER-a, and Fas receptor)
IR↓,
ER(estro)↓,
Fas↑,
PDGF↓, (PDGF, TGF, FGF, and EGF)
TGF-β↓,
FGF↓,
EGFR↓,
JAK↓,
PAK↓,
MAPK↓,
ATPase↓, (ATPase, COX-2, and matrix metalloproteinase enzyme [MMP])
COX2/PTGS2↓,
MMPs↓,
IL1↓, inflammatory cytokines (IL-1, IL-2, IL-5, IL-6, IL-8, IL-12, and IL-18)
IL2↓,
IL5↓,
IL6↓,
IL8↓,
IL12↓,
IL18↓,
NF-kB↓,
NOTCH1↓,
STAT1↓,
STAT4↓,
STAT5↓,
STAT3↓,

1863- dietFMD,  Chemo,    Effect of fasting on cancer: A narrative review of scientific evidence
- Review, Var, NA
eff↑, recommend combining prolonged periodic fasting with a standard conventional therapeutic approach to promote cancer‐free survival, treatment efficacy, and reduce side effects in cancer patients.
ChemoSideEff↓, lowered levels of IGF1 and insulin have the potential to protect healthy cells from side effects
ChemoSen↑,
Insulin↓, causes insulin levels to drop and glucagon levels to rise
HDAC↓, Histone deacetylases are inhibited by ketone bodies, which may slow tumor development.
IGF-1↓, FGF21 rises during intermittent fasting, and it plays a vital role in lowering IGF1 levels by inhibiting phosphorylated STAT5 in the liver
STAT5↓,
BG↓, Fasting suppresses glucose, IGF1, insulin, the MAPK pathway, and heme oxygenase 1
MAPK↓,
HO-1↓,
ATG3↑, while increasing many autophagy‐regulating components (Atgs, LC3, Beclin1, p62, Sirt1, and LAMP2).
Beclin-1↑,
p62↑,
SIRT1↑,
LAMP2↑,
OXPHOS↑, Fasting causes cancer cells to release oxidative phosphorylation (OXPHOS) through aerobic glycolysis
ROS↑, which leads to an increase in reactive oxygen species (ROS), p53 activation, DNA damage, and cell death in response to chemotherapy.
P53↑,
DNAdam↑,
TumCD↑,
ATP↑, and causes extracellular ATP accumulation, which inhibits Treg cells and the M2 phenotype while activating CD8+ cytotoxic T cells.
Treg lymp↓,
M2 MC↓,
CD8+↑,
Glycolysis↓, By lowering glucose intake and boosting fatty acid oxidation, fasting can induce a transition from aerobic glycolysis to mitochondrial oxidative phosphorylation in cancerous cells, resulting in increased ROS
GutMicro↑, Fasting has been shown to have a direct impact on the gut microbial community's constitution, function, and interaction with the host, which is the complex and diverse microbial population that lives in the intestine
GutMicro↑, Fasting also reduces the number of potentially harmful Proteobacteria while boosting the levels of Akkermansia muciniphila.
Warburg↓, Fasting generates an anti‐Warburg effect in colon cancer models, which increases oxygen demand but decreases ATP production, indicating an increase in mitochondrial uncoupling.
Dose↝, Those patients fasted for 36 h before treatment and 24 h thereafter, having a total of 350 calories per day. Within 8 days of chemotherapy, no substantial weight loss was recorded, although there was an improvement in quality of life and weariness.

6966- Form,    Formononetin-induced oxidative stress abrogates the activation of STAT3/5 signaling axis and suppresses the tumor growth in multiple myeloma preclinical model
- NA, MM, NA
tumCV↓, FT could significantly inhibit cell viability, and induce apoptosis.
Apoptosis↑,
STAT3↓, suppressed constitutive STAT3 (tyrosine residue 705 and serine residue 727) and STAT5 (tyrosine residue 694/699) activation
STAT5↓,
JAK1↓, correlated with the suppression of the upstream kinases (JAK1, JAK2, and c-Src) in MM cells
JAK2↓,
cSrc↓,
ROS↑, and this effect was found to be mediated via an increased production of reactive oxygen species (ROS) due to GSH/GSSG imbalance.
Casp3↑, induction of caspase-3 activation and cleavage of PARP
cl‑PARP↑,

7048- GA,    Natural bioactive gallic acid shows potential anticancer effects by inhibiting the proliferation and invasiveness behavior in human embryonic carcinoma cells
- in-vitro, Var, NA
AntiCan↑, Natural gallic acid (GA) is noted to have anticancer properties for oncogene expression, cycle arrest, apoptosis, angiogenesis, migration and metastasis in various cancers.
TumCCA↑,
angioG↓,
TumCMig↓,
TumMeta↓,
CSCs↓, In two types of embryonic CSCs, GA effectively induced cell death via late apoptosis
Apoptosis↑,
P21↑, GA showed the G0/G1 cell cycle arrest activity in embryonic CSCs by inducing the increase of p21, p27 and p53 expression and the decrease of CDK4, cyclin E and cyclin D1 expression.
P53↑,
p27/CDKN1B↑,
CDK4↓,
cycE/CCNE↓,
cycD1/CCND1↓,
SOX2↓, GA inhibited the expression levels of mRNA and protein for stem cell markers, such as SOX2, NANOG and OCT4, in NTERA-2 and NCCIT cells.
Nanog↓,
OCT4↓,
ROS↑, The induction of cellular and mitochondrial reactive oxygen species by GA also activated the cellular DNA damage response pathway by raising the phosphorylated-BRCA1, ATM, Chk1, Chk2 and histone.
DNAdam↑,
BRCA1↑,
ATM↑,
CHK1↑,
Chk2↑,
Histones↑,
TumCI↓, GA inhibited CSCs invasion and migration by inhibiting the expression of matrix metalloproteinase by the downregulation of EGFR/JAK2/STAT5 signaling pathway.
MMPs↓,
EGFR↓,
JAK2↓,
STAT5↓,

7067- GamB,    Gambogic Acid and Its Role in Chronic Diseases
- Review, Var, NA
*NF-kB↓, GA Inhibits Signaling of Nuclear Factor-Kappa B (NF-jB)
PI3K↓, GA Inhibits Phosphatidylinositol 3′-Kinase/Protein Kinase B (PI3K/Akt)
Akt↓,
STAT3↓, table 15.1 GA Inhibits Signal Transducer and Activator of Transcription-3 (STAT-3) Pathways
STAT5↓,
IL6↓,
COX2/PTGS2↓, GA Inhibits COX-2
iNOS↓, GA Inhibits iNOS
MMPs↓,
Src↓, GA Inhibits Src
PKA↓,
CXCR4↑, GA Inhibits Chemokine X-Receptor 4 (CXCR4) and Downstream Signaling Pathways
VEGF↓,
Bcl-2↓, GA Inhibits the Expression of Bcl-2 Family Proteins
Bcl-xL↓,
IAP1↓,
Mcl-1↓,
survivin↓,
cycD1/CCND1↓, GA Inhibits Expression of Cyclin D1
HSP90↓,
HSP70/HSPA5↓,
MAPK↓, GA Inhibits Mitogen-Activated Protein Kinase (MAPK)
HATs↓, GA Inhibits CBP/p300 Histone Aceyltransferase (HAT) and Histone Deacetylase (HDAC)
HDAC↓,
FAK↓, GA Inhibits the Activation of Focal Adhesion Kinase (FAK)
ROS↑, GA Induces the Production of Reactive Oxygen Species (ROS)
MMP7↓, GA Inhibits Matrix Metalloproteinase 7 & 9 (MMP-7 & 9)
MMP9↓,
α-tubulin↑, GA Inhibits Tubulin
cl‑PARP↑, GA Induces Cleavage of Poly(ADP-Ribose) Polymerases (PARPs)
TNF-α↓, GA Inhibits Tumor Necrosis Factor-a (TNF-a)
BID↑, GA Induces BID
BAD↑, GA Induces BAD
Cyt‑c↑, GA, induces the expression of cytochrome c in colorectal cancer HT-29, bladder cancer T24 and UMUC3, breast cancer MDA-MB-231, and human hepatocellular carcinoma cells
Casp3↑, GA Induces the Activation of Caspase-3 and Caspase-9
Casp9↑,
*AntiArt↑, GA inhibits RA by inhibiting the levels of cytokines and key inflammatory molecules [
*antiPs↑, recent study showed that GA could be used as an anti-psoriatic agent

7207- GBE,    The molecular mechanisms of ginkgo (Ginkgo biloba) activity in signaling pathways: A comprehensive review
- Review, AD, NA
*Inflam↓, G. biloba exerts its effects through its anti-inflammatory, anti-apoptotic, anti-cancer, neuroprotective, cardioprotective, hepatoprotective, antiviral, antibacterial, pulmoprotective, renoprotective, anti-osteoporosis, anti-melanogenic, ...
*Apoptosis↓,
*neuroP↑,
*cardioP↑,
*hepatoP↑,
*AntiViral↑,
*Bacteria↓,
*RenoP↑,
*ROS↓, The most important mechanisms involved in these actions are altering the elevation of ROS formation, inhibiting NADPH oxidases activation
*NADPH↓,
*MAPK↓, downregulating MAPKs (p38 MAPK and ERK, and JNK) and AP-1, increasing cAMP, inactivating Stat5,
*ERK↓,
*JNK↓,
*AP-1↓,
*cAMP↑,
*STAT5↓,
*AMPK↑, activating the AMPK signaling pathway

1070- IVM,    Ivermectin accelerates autophagic death of glioma cells by inhibiting glycolysis through blocking GLUT4 mediated JAK/STAT signaling pathway activation
- vitro+vivo, GBM, NA
TumCG↓,
LC3II↑,
p62↓,
ATP↓,
Pyruv↓,
GlucoseCon↑, promoted glucose uptake
HK2↓,
PFK1↓,
GLUT4↓,
Glycolysis↓,
JAK2↓,
p‑STAT3↓,
p‑STAT5↓,

1203- MSM,    Methylsulfonylmethane Suppresses Breast Cancer Growth by Down-Regulating STAT3 and STAT5b Pathways
- vitro+vivo, BC, MDA-MB-231
tumCV↓,
STAT3↓,
STAT5↓, STAT5b
IGF-1↓,
Hif1a↓,
VEGF↓,
Brk/PTK6↓,
IGF-1R↓,

3098- RES,    Regulation of Cell Signaling Pathways and miRNAs by Resveratrol in Different Cancers
- Review, Var, NA
NOTCH2↓, resveratrol has been reported to target multiple proteins in ovarian cancer, markedly reducing NOTCH2 and HES1 in OVCAR-3 and CAOV-3 cells
Wnt↓, In CAOV-3 cells, resveratrol downregulated WNT2 and reduced the nuclear accumulation of β-catenin
β-catenin/ZEB1↓,
p‑SMAD2↓, Resveratrol effectively inhibits SMAD proteins
p‑SMAD3↓, Resveratrol has been reported to reduce phosphorylated-SMAD2/3 in colorectal cancer LoVo cells
PTCH1↓, PTCH, SMO, and GLI-1 were also inhibited in resveratrol-treated colorectal cancer HCT116 cells
Smo↓,
Gli1↓,
E-cadherin↑, resveratrol upregulated E-cadherin
NOTCH⇅, Although some reports document efficient inhibition of different proteins of the NOTCH pathway by resveratrol to inhibit cancer, there are conflicting reports that resveratrol can activate the NOTCH pathway, leading to its anticancer activity.
TAC?,
NKG2D↑, Resveratrol has been found to increase the cell-surface expression of NKG2D ligands and DR4 along
DR4↑,
survivin↓, Resveratrol dose-dependently downregulated survivin in HepG2 cells.
DR5↑, resveratrol upregulated DR4, DR5, Bax, and p27(/KIP1) and inhibited the expression of cyclin D1 and Bcl-2
BAX↑,
p27/CDKN1B↑,
cycD1/CCND1↓,
Bcl-2↓,
STAT3↓, Resveratrol exerts inhibitory effects on the constitutive activation of STAT3 and STAT5.
STAT5↓,
JAK↓, Resveratrol has also been shown to prevent the activation of JAK,
DNAdam↑, Resveratrol induced DNA damage, as evidenced by the presence of multiple γ-H2AX foci after treatment with 25 μM resveratrol.
γH2AX↑,

978- SIL,    A comprehensive evaluation of the therapeutic potential of silibinin: a ray of hope in cancer treatment
- Review, NA, NA
PI3K↓,
Akt↓,
NF-kB↓,
Wnt/(β-catenin)↓,
MAPK↓,
TumCP↓,
TumCCA↑, G0/G1 cell cycle arrest
Apoptosis↑, In T24 and UM-UC-3 human bladder cancer cells, silibinin treatment at a concentration of 10 μM significantly inhibited proliferation, migration, invasion, and induced apoptosis.
p‑EGFR↓,
JAK2↓,
STAT5↓,
cycD1/CCND1↓,
hTERT/TERT↓,
AP-1↓,
MMP9↓,
miR-21↓,
miR-155↓,
Casp9↑,
BID↑,
ERK↓, ERK1/2
Akt2↓,
DNMT1↓,
P53↑,
survivin↓,
Casp3↑,
ROS↑, cytotoxicity of silibinin in Hep-2 cells was associated with the accumulation of intracellular reactive oxygen species (ROS), which could be mitigated by the ROS scavenger NAC.


Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

HO-1↓, 1,   NRF2↑, 1,   OXPHOS↑, 1,   ROS↑, 5,   TAC?, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   ATP↑, 1,   Insulin↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

p‑CREB↓, 1,   GlucoseCon↑, 1,   Glycolysis↓, 2,   Histones↑, 1,   HK2↓, 1,   IR↓, 1,   PFK1↓, 1,   PPARγ↑, 1,   Pyruv↓, 1,   SIRT1↑, 1,   Warburg↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 5,   BAD↑, 1,   BAX↑, 1,   Bcl-2↓, 2,   Bcl-xL↓, 2,   BID↑, 2,   Casp3↑, 4,   Casp9↑, 2,   Chk2↑, 1,   p‑Chk2↓, 1,   Cyt‑c↑, 1,   DR4↑, 1,   DR5↑, 2,   Fas↑, 1,   hTERT/TERT↓, 1,   IAP1↓, 1,   iNOS↓, 1,   JNK↑, 1,   MAPK↓, 4,   Mcl-1↓, 1,   p27/CDKN1B↑, 2,   p‑p38↓, 1,   p‑RSK↓, 1,   survivin↓, 3,   TumCD↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

cSrc↓, 1,   HER2/EBBR2↓, 1,   PAK↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

HATs↓, 1,   miR-21↓, 1,   tumCV↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

HSP70/HSPA5↓, 1,   HSP90↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG3↑, 1,   Beclin-1↑, 1,   LAMP2↑, 1,   LC3II↑, 1,   p62↓, 1,   p62↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,   BRCA1↑, 1,   CHK1↑, 1,   DNAdam↑, 3,   DNMT1↓, 1,   P53↑, 4,   cl‑PARP↑, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   cycA1/CCNA1↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 4,   cycE/CCNE↓, 1,   P21↑, 2,   TumCCA↑, 3,  

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

CSCs↓, 1,   ERK↓, 1,   p‑ERK↓, 1,   FGF↓, 1,   Gli1↓, 1,   HDAC↓, 2,   IGF-1↓, 2,   IGF-1R↓, 1,   Nanog↓, 1,   NOTCH⇅, 1,   NOTCH1↓, 1,   NOTCH2↓, 1,   OCT4↓, 1,   PI3K↓, 2,   PTCH1↓, 1,   Smo↓, 1,   SOX2↓, 1,   Src↓, 1,   STAT1↓, 1,   STAT3↓, 6,   p‑STAT3↓, 1,   STAT4↓, 1,   STAT5↓, 9,   p‑STAT5↓, 2,   TumCG↓, 2,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

Akt2↓, 1,   AP-1↓, 1,   ATPase↓, 1,   Brk/PTK6↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   miR-155↓, 1,   MMP7↓, 1,   MMP9↓, 2,   MMPs↓, 3,   PDGF↓, 1,   PKA↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   TGF-β↓, 1,   Treg lymp↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 1,   α-tubulin↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   EGFR↓, 2,   p‑EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Barriers & Transport(tgid=15) ⓘ

GLUT4↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2,   CXCR4↑, 1,   IL1↓, 1,   IL12↓, 1,   IL18↓, 1,   IL2↓, 1,   IL5↓, 1,   IL6↓, 2,   IL8↓, 1,   JAK↓, 2,   JAK1↓, 1,   JAK2↓, 5,   M2 MC↓, 1,   NF-kB↓, 2,   SOCS1↑, 1,   TNF-α↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

ER(estro)↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 2,   Dose↝, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BG↓, 1,   BRCA1↑, 1,   EGFR↓, 2,   p‑EGFR↓, 1,   GutMicro↑, 2,   HER2/EBBR2↓, 1,   hTERT/TERT↓, 1,   IL6↓, 2,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   ChemoSideEff↓, 1,   NKG2D↑, 1,   toxicity↓, 1,   TumVol↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

CD8+↑, 1,  
Total Targets: 163

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiArt↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,   cAMP↑, 1,   NADPH↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,   JNK↓, 1,   MAPK↓, 1,  

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

ERK↓, 1,   STAT5↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Functional Outcomes(tgid=23) ⓘ

antiPs↑, 1,   cardioP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   RenoP↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 1,  
Total Targets: 20

Scientific Paper Hit Count for: STAT5, Signal transducer and activator of transcription 5
1 Artemisinin
1 Cucurbitacin
1 Curcumin
1 diet FMD Fasting Mimicking Diet
1 Chemotherapy
1 Formononetin
1 Gallic acid
1 Gambogic Acid
1 Ginkgo biloba
1 Ivermectin
1 Methylsulfonylmethane
1 Resveratrol
1 Silymarin (Milk Thistle) silibinin
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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