mTORC1 restricts hepatitis C virus RNA replication through ULK1-mediated suppression of miR-122 and facilitates post-replication events.

The mechanistic target of rapamycin (mTOR), an important kinase that assimilates several upstream signals, associates into two functional complexes, mTORC1 and mTORC2. In this study, we demonstrate that HCV infection activates mTORC1 that functions in important antiviral response. Pharmacological inhibition of mTOR complexes augmented cellular HCV RNA levels, the observation confirmed further by Raptor depletion, indicating antiviral roles of mTORC1.

An Atypical System for Studying Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma.

Intrahepatic and extrahepatic metastases are frequently detected in hepatocellular carcinoma (HCC). Epithelial-mesenchymal transition (EMT) is believed to drive metastasis. There are not many well-established model systems to study EMT in HCC.