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↑,

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↓,
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.

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↑,
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 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↓, 1,   NRF2↑, 1,   OXPHOS↑, 1,   ROS↑, 2,   TAC?, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ATP↑, 1,   Insulin↓, 1,  

Core Metabolism/Glycolysis ⓘ

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

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   BID↑, 1,   Casp3↑, 2,   Casp9↑, 1,   p‑Chk2↓, 1,   DR4↑, 1,   DR5↑, 2,   Fas↑, 1,   hTERT/TERT↓, 1,   JNK↑, 1,   MAPK↓, 3,   p27↑, 1,   p‑p38↓, 1,   p‑RSK↓, 1,   survivin↓, 2,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   PAK↓, 1,  

Transcription & Epigenetics ⓘ

miR-21↓, 1,   tumCV↓, 1,  

Autophagy & Lysosomes ⓘ

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

DNA Damage & Repair ⓘ

DNAdam↑, 2,   DNMT1↓, 1,   P53↑, 3,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 2,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   p‑ERK↓, 1,   FGF↓, 1,   Gli1↓, 1,   HDAC↓, 1,   IGF-1↓, 2,   IGF-1R↓, 1,   NOTCH⇅, 1,   NOTCH1↓, 1,   NOTCH2↓, 1,   PI3K↓, 1,   PTCH1↓, 1,   Smo↓, 1,   STAT1↓, 1,   STAT3↓, 3,   p‑STAT3↓, 1,   STAT4↓, 1,   STAT5↓, 5,   p‑STAT5↓, 2,   TumCG↓, 1,   Wnt↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

Akt2↓, 1,   AP-1↓, 1,   ATPase↓, 1,   Brk/PTK6↓, 1,   E-cadherin↑, 1,   miR-155↓, 1,   MMP9↓, 1,   MMPs↓, 1,   PDGF↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↓, 1,   TGF-β↓, 1,   Treg lymp↓, 1,   TumCP↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

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

Barriers & Transport ⓘ

GLUT4↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL1↓, 1,   IL12↓, 1,   IL18↓, 1,   IL2↓, 1,   IL5↓, 1,   IL6↓, 1,   IL8↓, 1,   JAK↓, 2,   JAK2↓, 2,   M2 MC↓, 1,   NF-kB↓, 2,   SOCS1↑, 1,  

Hormonal & Nuclear Receptors ⓘ

ER(estro)↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

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

Functional Outcomes ⓘ

ChemoSideEff↓, 1,   NKG2D↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 122

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: STAT5, Signal transducer and activator of transcription 5
1 Artemisinin
1 Curcumin
1 diet FMD Fasting Mimicking Diet
1 Chemotherapy
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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