https://www.selleckchem.com/products/ars-1620.html
In mice overexpressing a myristoylated/activated form of AKT, co-expression of SMAD7 accelerated carcinogenesis and switched the phenotype from HCC to intrahepatic cholangiocarcinoma (iCCA) lesions. In human iCCA, SMAD7 expression was robustly upregulated, especially in the most aggressive tumors and directly correlated with the levels of YAP/NOTCH targets as well as cholangiocellular and EMT markers. The present data indicate that SMAD7 contributes to liver carcinogenesis by activating the YAP/NOTCH signaling cascade and by inducing a