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HGF — STAT3

Text-mined interactions from Literome

Hung et al., J Biol Chem 2001 (Mammary Neoplasms, Experimental) : Coexpression of activated c-Src and Stat3 synergistically induced strong HGF promoter activity in SP1 cells, as well as in a nonmalignant epithelial cell line, HC11 ( HGF negative )
Elliott et al., Can J Physiol Pharmacol 2002 (Breast Neoplasms...) : We have recently demonstrated that sustained activation or hyper-activation of c-Src and Stat3 , which occurs in invasive breast cancer, can stimulate strong expression of HGF in carcinoma cells
Song et al., Oncogene 2003 (Carcinoma, Non-Small-Cell Lung...) : Furthermore, the stimulation of Stat3 DNA binding activity by EGF requires the activity of EGF-R tyrosine kinase as well as Src-kinase, while the upregulation of Stat3 activity by IL-6 or HGF requires only Src-kinase activity
Tokumaru et al., Biochem Biophys Res Commun 2005 : Transfection with the dominant negative mutant of STAT3 almost completely abolished HGF induced keratinocyte migration and STAT3 phosphorylation ... Transfection with SOCS3/CIS3 almost completely abolished HGF induced STAT3 phosphorylation and keratinocyte migration, indicating that SOCS3/CIS3 acts as a negative regulator of HGF induced keratinocyte migration
Tsukiyama et al., Tissue Eng 2006 : Stat3-C induced cell proliferation of beta-cells without loss of insulin secretion activity at the glucose challenge, and HGF enhanced the beta-cell proliferative activity of Stat3-C
Sam et al., Molecular cancer 2007 (Breast Neoplasms) : A novel activating role of SRC and STAT3 on HGF transcription in human breast cancer cells ... The exception was the ErbB2 over expressing cell line SK-BR-3 where Stat3 alone could transactivate HGF though Src augmented this effect ... Src/Stat3 expression did activate HGF transcription in OVCAR3 cells, but this effect was not mediated by the Stat3 site at nt-95 ... These results suggest that human breast cells are a uniquely permissive environment for HGF transactivation by Src/Stat3 which may allow for the inappropriate activation of HGF transcription during the early stages of breast transformation
Seki et al., J Hepatol 2008 : Since HGF and EGF can activate STAT3 via gp130 independent MET and EGFR, respectively, we assumed that these factors account for STAT3 dependent liver regeneration ... Hepatocytes infected with socs1-virus lacked STAT3 phosphorylation in response to IL-6 and HGF , while cells infected with socs3-virus lacked the response to all of IL-6, HGF and EGF, indicating that those SOCS proteins differently regulate EGFR signaling
Syed et al., Toxicol Appl Pharmacol 2008 (Breast Neoplasms...) : Inhibition of HGF mediated membrane translocation of PKCalpha as well as decreased phosphorylation of STAT3 was further observed in delphinidin treated cells
Wang et al., J Biol Chem 2008 : Interestingly, the expression of the IGF2 gene and the HGF gene is also regulated by JAK2/STAT2/STAT3 , suggesting that this pathway could also promote differentiation by regulating signaling molecules known to be involved in myogenic differentiation
Lee et al., Cell Signal 2009 : Hepatocyte growth factor induces delayed STAT3 phosphorylation through interleukin-6 expression
Nechemia-Arbely et al., J Hepatol 2011 : This cooperative effect correlated with greater resistance of HIL-6 than IL-6 to HGF mediated reduction of AKT activation, rather than changes in STAT3 or MAPK signaling, and was completely blocked by PI3K inhibition
Garnett et al., Neoplasia (New York, N.Y.) 2013 (Brain Neoplasms...) : Suppression of STAT3 phosphorylation with WP1193 reduced HGF expression in dEGFR expressing GBM cells, whereas constitutively active STAT3 partially rescued HGF expression and colony formation in c-Met knockdown cells expressing dEGFR ... These results suggest that the c-Met/HGF signaling axis is enhanced by dEGFR through increased STAT3 dependent HGF expression and that targeting c-Met in Mes GBMs may be an important strategy for therapy