IndraLab

"Inhibition of c-Met by PHA-665752 suppressed the phosphorylation of c-Met, Akt, Cortactin and STAT3 (Fig. 8C)."

"Another study shows that HGF/c-Met could phosphorylate STAT3 and then promote Bcl-2 transcription, underlying the anti-apoptotic effect as an upstream signal [91]."

"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."

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

"Upregulation of c-MET may increase the expression and phosphorylation of STAT3, wherein the activated STAT3 directly regulates genes involved in proliferation (including cyclin D1, c-Myc, p53 and p21), survival (including Bcl-2, Bcl-xL, MCL1 apoptosis regulator and survivin), metastasis (including MMP2 and MMP9) and angiogenesis (including vascular endothelial growth factor) in numerous types of cancer."

"In addition, the induction of epi- Kinase upregulation 1234 Y Y 1235 P P Tyrosine kinase domain thelial tubules by HGF is dependent on activation of the STAT pathway, and of importance, c-met can bind and directly phosphorylate STAT3 [14]."

"With EGF stimulation, Pyk2 affects STAT3 phosphorylation and the protein and mRNA levels of c-Met, c-Met enhances the phosphorylation of Pyk2 and STAT3 and also STAT3 regulates Pyk2 transcription and c-Met expression in human breast carcinoma, forming a positive feedback in the PYK2-STAT3-c-Met axis that contributes to cancer metastasis and prolongs EMT-associated signals in breast cancer [ xref ]."

"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."

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

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

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

"With EGF stimulation, Pyk2 affects STAT3 phosphorylation and the protein and mRNA levels of c-Met, c-Met enhances the phosphorylation of Pyk2 and STAT3 and also STAT3 regulates Pyk2 transcription and c-Met expression in human breast carcinoma, forming a positive feedback in the PYK2-STAT3-c-Met axis that contributes to cancer metastasis and prolongs EMT-associated signals in breast cancer [12]."

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

"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)."

"This loop also enhanced the expression of c-Met, which induces PYK2 and STAT3 phosphorylation in response to hepatocyte growth factor (HGF) and can also transphosphorylate EGFR to sustain its activati[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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

"The study demonstrated that the HGF receptor binds and phosphorylates Stat-3 and that the ensuing nuclear signaling is required to trigger differentiation for branching morphogenesis ( xref )."

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