https://www.selleckchem.com/products/dup-697.html
We further showed that LISCH7 could directly bind to the TGFB1 promoter and stimulate TGFB1 transcription in TNBC cells. The recruitment of LISCH7 onto the TGFB1 chromatin and transactivation of TGFB1 were substantially augmented by treatment with the exogenous TGF-β1 in a time- and dose-dependent manner. Collectively, these findings suggest that LISCH7 and TGF-β1 form a reciprocal positive regulatory loop and cooperatively regulate cancerous progression in TNBC cells. Thus, simultaneous inhibition of both LISCH7 and TGF-β1 signaling ma
Like
Comment
Share
