ArticleBritish journal of cancer2011
Differential roles of STAT3 depending on the mechanism of STAT3 activation in gastric cancer cells.
Article in British journal of cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Association between STAT3 polymorphisms and cancer risk: a meta-analysis.Molecular genetics and genomics : MGG · 2015Pooled it
- SOCS3 gene silencing does not occur through methylation and mutations in gastric cancer.Human cell · 2022Article
- Blockage of ETS homologous factor inhibits the proliferation and invasion of gastric cancer cells through the c-Met pathway.World journal of gastroenterology · 2020Article
- IL‑10 secreted by cancer‑associated macrophages regulates proliferation and invasion in gastric cancer cells via c‑Met/STAT3 signaling.Oncology reports · 2019Article
- RNAi-mediated silencing of NOX4 inhibited the invasion of gastric cancer cells through JAK2/STAT3 signaling.American journal of translational research · 2017Article
- Article
- Fas Signaling Promotes Gastric Cancer Metastasis through STAT3-Dependent Upregulation of Fascin.PloS one · 2015Article
- Molecular targeting to treat gastric cancer.World journal of gastroenterology · 2014Review
- Genetic modulation of the interleukin 6 (IL-6) system in patients with advanced gastric cancer: a background for an alternative target therapy.BMC cancer · 2014Article
- Signal transducer and activator of transcription 3 signaling upregulates fascin via nuclear factor-κB in gastric cancer: Implications in cell invasion and migration.Oncology letters · 2014Article
- rs744166 polymorphism of the STAT3 gene is associated with risk of gastric cancer in a Chinese population.BioMed research international · 2014Article
- AXL and MET crosstalk to promote gonadotropin releasing hormone (GnRH) neuronal cell migration and survival.Molecular and cellular endocrinology · 2013Article
- A synergistic interaction between transcription factors nuclear factor-κB and signal transducers and activators of transcription 3 promotes gastric cancer cell migration and invasion.BMC gastroenterology · 2013Article
- Interleukin-6 mediates epithelial-stromal interactions and promotes gastric tumorigenesis.PloS one · 2013Article
- Proteinase-activated receptor 2 (PAR(2)) in cholangiocarcinoma (CCA) cells: effects on signaling and cellular level.Histochemistry and cell biology · 2012Article
- STAT3 can serve as a hit in the process of malignant transformation of primary cells.Cell death and differentiation · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSignal transducer and activator of transcription 3 (STAT3) is a transcription factor that is activated in response to growth factors and cytokines, and which contributes to the regulation of cell proliferation, apoptosis, and motility in many human tumour types.
methodsWe investigated the mechanisms of STAT3 activation and the function of STAT3 depending on its mechanism of activation in gastric cancer cells.
resultsThe MET-tyrosine kinase inhibitor (TKI) and cell transfection with a small interfering RNA (siRNA) specific for MET mRNA inhibited STAT3 phosphorylation in MET-activated cells, indicating that STAT3 activation is linked to MET signalling. Forced expression of a constitutively active form of STAT3 also attenuated MET-TKI-induced apoptosis, suggesting that inhibition of STAT3 activity contributes to MET-TKI-induced apoptosis. MKN1 and MKN7 cells, both of which are negative for MET activation, produced interleukin-6 (IL-6) that activated STAT3 through the Janus kinase pathway. Depletion of STAT3 by siRNA inhibited migration and invasion of these cells, suggesting that STAT3 activated by IL-6 contributes to regulation of cell motility.
conclusionOur data thus show that activated STAT3 contributes to either cell survival or motility in gastric cancer cells, and that these actions are related to different mechanisms of STAT3 activation.
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