ArticleBMC cancer2011
HGF/c-met/Stat3 signaling during skin tumor cell invasion: indications for a positive feedback loop.
Article in BMC cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- Mechanistic insights into c-Met rs368750834 mutation and a bifunctional CAR-T strategy for serous ovarian carcinoma.Journal of ovarian research · 2025Article
- Double-sided niche regulation in skin stem cell and cancer: mechanisms and clinical applications.Molecular cancer · 2025Review
- Nuclear transport of phosphorylated LanCL2 promotes invadopodia formation and tumor progression of glioblastoma by activating STAT3/Cortactin signaling.Journal of advanced research · 2025Article
- Targeting HGF/c-MET signaling to regulate the tumor microenvironment: Implications for counteracting tumor immune evasion.Cell communication and signaling : CCS · 2025Review
- Epithelial tubule interconnection driven by HGF-Met signaling in the kidney.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Epithelial tubule interconnection driven by HGF-Met signaling in the kidney.bioRxiv : the preprint server for biology · 2024Article
- Review
- HGF/c-Met/β1-integrin signalling axis induces tunneling nanotubes in A549 lung adenocarcinoma cells.Life science alliance · 2023Article
- Matrix from urine stem cells boosts tissue-specific stem cell mediated functional cartilage reconstruction.Bioactive materials · 2023Article
- Differential responses to immune checkpoint inhibitor dictated by pre-existing differential immune profiles in squamous cell carcinomas caused by same initial oncogenic drivers.Journal of experimental & clinical cancer research : CR · 2022Article
- Transglutaminase 2 Maintains Hepatocyte Growth Factor Signaling to Enhance the Cancer Cell Phenotype.Molecular cancer research : MCR · 2021Article
- IL‑10 secreted by cancer‑associated macrophages regulates proliferation and invasion in gastric cancer cells via c‑Met/STAT3 signaling.Oncology reports · 2019Article
- SDF-1α promotes repair of myocardial ischemic necrosis zones in rats.International journal of clinical and experimental pathology · 2019Article
- Extracellular Matrix Influencing HGF/c-MET Signaling Pathway: Impact on Cancer Progression.International journal of molecular sciences · 2018Review
- PI3K/AKT inhibition induces compensatory activation of the MET/STAT3 pathway in non-small cell lung cancer.Oncology letters · 2018Article
- Activation of the HGF/c-Met axis in the tumor microenvironment: A multispecies model.Journal of theoretical biology · 2018Article
- BPI-9016M, a c-Met inhibitor, suppresses tumor cell growth, migration and invasion of lung adenocarcinoma via miR203-DKK1.Theranostics · 2018Article
- Luteolin selectively kills STAT3 highly activated gastric cancer cells through enhancing the binding of STAT3 to SHP-1.Cell death & disease · 2017Article
- Hepatocyte growth factor induces breast cancer cell invasion via the PI3K/Akt and p38 MAPK signaling pathways to up-regulate the expression of COX2.American journal of translational research · 2017Article
- MET: roles in epithelial-mesenchymal transition and cancer stemness.Annals of translational medicine · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundStat3 is a cytokine- and growth factor-inducible transcription factor that regulates cell motility, migration, and invasion under normal and pathological situations, making it a promising target for cancer therapeutics. The hepatocyte growth factor (HGF)/c-met receptor tyrosine kinase signaling pathway is responsible for stimulation of cell motility and invasion, and Stat3 is responsible for at least part of the c-met signal.
methodsWe have stably transfected a human squamous cell carcinoma (SCC) cell line (SRB12-p9) to force the expression of a dominant negative form of Stat3 (S3DN), which we have previously shown to suppress Stat3 activity. The in vitro and in vivo malignant behavior of the S3DN cells was compared to parental and vector transfected controls.
resultsSuppression of Stat3 activity impaired the ability of the S3DN cells to scatter upon stimulation with HGF (c-met ligand), enhanced their adhesion, and diminished their capacity to invade in vitro and in vivo. Surprisingly, S3DN cells also showed suppressed HGF-induced activation of c-met, and had nearly undetectable basal c-met activity, as revealed by a phospho-specific c-met antibody. In addition, we showed that there is a strong membrane specific localization of phospho-Stat3 in the wild type (WT) and vector transfected control (NEO4) SRB12-p9 cells, which is lost in the S3DN cells. Finally, co-immunoprecipitation experiments revealed that S3DN interfered with Stat3/c-met interaction.
conclusionThese studies are the first confirm that interference with the HGF/c-met/Stat3 signaling pathway can block tumor cell invasion in an in vivo model. We also provide novel evidence for a possible positive feedback loop whereby Stat3 can activate c-met, and we correlate membrane localization of phospho-Stat3 with invasion in vivo.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.