ArticleOncogene2006
A novel activating function of c-Src and Stat3 on HGF transcription in mammary carcinoma cells.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 61 citations in OpenAlex.
- High expression of STAT3 within the tumour-associated stroma predicts poor outcome in breast cancer patients.Cancer medicine · 2023Article
- Article
- Highlighted STAT3 as a potential drug target for cancer therapy.BMB reports · 2019Review
- The role of STAT3 in leading the crosstalk between human cancers and the immune system.Cancer letters · 2018Review
- Pancreatic islet hepatocyte growth factor and vascular endothelial growth factor A signaling in growth restricted fetuses.Molecular and cellular endocrinology · 2016Review
- The Therapeutic Potential of Targeting the HGF/cMET Axis in Ovarian Cancer.Molecular diagnosis & therapy · 2016Review
- Mesenchymal Stem Cell Exosomes Induce Proliferation and Migration of Normal and Chronic Wound Fibroblasts, and Enhance Angiogenesis In Vitro.Stem cells and development · 2015Article
- The Cytokinome Profile in Patients with Hepatocellular Carcinoma and Type 2 Diabetes.PloS one · 2015Article
- MLS-2384, a new 6-bromoindirubin derivative with dual JAK/Src kinase inhibitory activity, suppresses growth of diverse cancer cells.Cancer biology & therapy · 2014Article
- Profiling phospho-signaling networks in breast cancer using reverse-phase protein arrays.Oncogene · 2013Article
- Regulation of HGF expression by ΔEGFR-mediated c-Met activation in glioblastoma cells.Neoplasia (New York, N.Y.) · 2013Article
- A novel 7-bromoindirubin with potent anticancer activity suppresses survival of human melanoma cells associated with inhibition of STAT3 and Akt signaling.Cancer biology & therapy · 2012Article
- Metabolic stress, reactive oxygen species, and arrhythmia.Journal of molecular and cellular cardiology · 2012Review
- Inhibition of c-Src tyrosine kinase prevents angiotensin II-mediated connexin-43 remodeling and sudden cardiac death.Journal of the American College of Cardiology · 2011Article
- Essential role of Stat3 in PI3K-induced oncogenic transformation.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- HGF/c-met/Stat3 signaling during skin tumor cell invasion: indications for a positive feedback loop.BMC cancer · 2011Article
- RhoA-mediated signaling up-regulates hepatocyte growth factor gene and protein expression in response to apoptotic cells.Journal of leukocyte biology · 2011Article
- Activation of host tissue trophic factors through JAK-STAT3 signaling: a mechanism of mesenchymal stem cell-mediated cardiac repair.American journal of physiology. Heart and circulatory physiology · 2010Article
- [The roles of signal transducer and activator of transcription 3 in tumor metastasis].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2010Review
- Role of Src signal transduction pathways in scatter factor-mediated cellular protection.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the normal breast, hepatocyte growth factor (HGF) is primarily expressed by stromal cells, and stimulates in a paracrine manner epithelial cells expressing the HGF receptor (Met). In invasive human breast carcinomas, HGF and Met are frequently overexpressed, possibly establishing an autocrine HGF/Met loop that promotes tumour cell invasion. However, the mechanisms leading to autocrine HGF expression in carcinoma cells are not known. We previously demonstrated a cooperative effect between c-Src and Stat3 in the activation of HGF transcription in mammary carcinoma cells. The present report defines a novel Stat3 consensus site at nt -95 in the HGF promoter that is highly conserved in human and mouse, and is required for c-Src and Stat3 to activate HGF transcription in breast epithelial cells. DNA-protein binding studies demonstrated high affinity binding of a Stat3-containing complex to the nt -95 site. Endogenous Stat3 binding to this region of the HGF promoter in carcinoma cells expressing HGF was demonstrated using a chromatin immunoprecipitation assay. In addition, coexpression of Stat3 and activated c-Src caused increased expression of endogenous HGF mRNA and protein and marked cell scattering in breast epithelial cells. Our results delineate a novel c-Src/Stat3-dependent mechanism that regulates HGF promoter activity, and is linked to transformation of mammary epithelial cells.
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Registered trials
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.