IndraLab

"Upon MEK inhibitor treatment, c-MET, but not IL-6, upregulates phosphorylation of STAT3."

"Activated c-Met directly phosphorylates STAT3 [ xref ]."

"Receptor tyrosine kinases, EGFR and c-Met, phosphorylate Stat3 upon ligand binding."

"The overexpression of c-Met promoted MGMT expression and phosphorylation of Stat3 and MAPK (Supplementary Fig. 6e, f)."

"Thus, HGF mediates the expansion of MDSCs by binding to its receptor, c-Met, which leads to increased phosphorylation of STAT3 (XREF_FIG)."

"Activation of cell surface receptor tyrosine kinases AXL and c-MET induces AKT, ERK, and STAT-3 phosphorylation, which contributes to sunitinib resistance in RCC cells. xref Furthermore, chemotherapeutic drugs, including sorafenib, camptothecin, and doxorubicin, induce lncRNA VLDLR antisense RNA 1 (VLDLR) in HCC cells that contribute to drug resistance. xref Drug-resistant HCC cells release lncRNA VLDLR in exosomes that promote resistance in recipient drug-sensitive HCC cells by promoting the expression of ATP-binding cassette (ABC) transporters, including ABCG2 (ATP-binding cassette, subfamily G member 2). xref ABC transporters pump a variety of drugs out of cells at the expense of ATP hydrolysis. xref Furthermore, mesenchymal stem cells induce proteasomal inhibitor and chemotherapy drug bortezomib resistance in multiple myeloma cells by secreting proteasome subunit α3 (PSMA3) and lncRNA PSMA3-AS1 (arises from the antisense strand of PSMA3) in exosomes. xref PSMA3 mRNA forms a duplex with the lncRNA PSMA3-AS1 transcript that promotes PSMA3 mRNA stability by reducing its decay."

"This effect may correlate with the activity of receptor molecules since c-met activates the phosphorylation of stat3."

"We also showed that inhibition of c-Met using a specific inhibitor (PHA-665752) reduced the phosphorylation of both PYK2 and STAT3 in response to EGFR stimulation [XREF_BIBR], while STAT3 inhibition decreased c-Met transcription, suggesting that STAT3 enhances the transcription of c-Met (reaction 13)."

"It has been reported that c-Met can activate STAT3 at the endosome and phosphorylated STAT3 induced by c-Met is colocalized with EEA1, an early endosome marker."

"This effect may correlate with the activity of receptor molecules since c-met activates the phosphorylation of stat3."

"# Ariadne: Stat3 activation by the hepatocyte growth factor/scatter factor receptor c-Met has been shown to be involved in epithelial tubule formation. [Regulation]"