Abstract 3547: CEBPD induces apoptosis through autophagy in metformin-treated HCC

Abstract

Abstract The patients with hepatocellular carcinoma (HCC) face the risk of cancer relapse or liver dysfunction. Metformin (Met), a first-line drug of type 2 diabetes, has been proved that it could induce G1 arrest and prevent or inhibit HCC. Previously, we demonstrated that the transcription factor CCAAT/enhancer-binding protein delta (CEBPD) plays a tumor suppressor and is responsive to many anticancer drugs in HCC. In this study, we found that Met could induce autophagy, growth arrest and further apoptosis in Huh7 cells. Met enhanced CEBPD expression via stabilizing its protein stability. The loss of CEBPD attenuated the Met-induced autophagy, growth arrest and apoptosis. Importantly, in addition to increasing P27 and down-regulating cyclin D1, CEBPD also contributed the increases of LC3B and ATG3 and LC3 puncta formation. We revealed a novel involvement of CEBPD in Met-induced growth arrest, apoptosis and autophagy of liver cancer cells through regulating p27, cyclinD1, LC3B and ATG3. Citation Format: I P. Lin. CEBPD induces apoptosis through autophagy in metformin-treated HCC. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 3547.