https://www.selleckchem.com/products/ve-821.html
Mechanistically, results of Chromatin immunoprecipitation (ChIP) and immunoblotting assays revealed that HSF4 associated directly to MET promoter to enhance expression of c-MET, a well-known oncogene in multiple cancers, thus fueling the activity of downstream ERK1/2 and AKT signaling pathways. In further rescue experiments, restoration of c-MET expression abolished inhibitory cell growth and invasion induced by downregulated HSF4 expression. To sum up, our findings describe a crucial role of HSF4 in CRC progression by enhancing activity
Like
Comment
Share
