Galunisertib suppresses the staminal phenotype in hepatocellular carcinoma by modulating CD44 expression.

ABSTRACT: Cancer stem cells (CSCs) niche in the tumor microenvironment is responsible for cancer recurrence and therapy failure. To better understand its molecular and biological involvement in hepatocellular carcinoma (HCC) progression, one can design more effective therapies and tailored then to individual patients. While sorafenib is currently the only approved drug for first-line treatment of advanced stage HCC, its role in modulating the CSC niche is estimated to be small. By contrast, transforming growth factor (TGF)-β pathway seems to influence the CSC and thus may impact hallmarks of HCC, such as liver fibrosis, cirrhosis, and tumor progression. Therefore, blocking this pathway may offer an appealing and druggable target. In our study, we have used galunisertib (LY2157299), a selective ATP-m

SUBMITTER: Rani B 

PROVIDER: S-EPMC5841307 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature