J Cancer 2017; 8(7):1205-1213. doi:10.7150/jca.18255


E2F8 is a Potential Therapeutic Target for Hepatocellular Carcinoma

Yi Lv1, 2, Jia Xiao 1, Jing Liu3✉, Feiyue Xing1, 2✉

1. Department of Immunobiology, Institute of Tissue Transplantation and Immunology, Jinan University, Guangzhou, China;
2. Key Laboratory of Functional Protein Research of Guangdong, Higher Education Institutes, Jinan University, Guangzhou, China;
3. Department of Stomatology, Jinan University, Guangzhou, China.


E2F transcriptional factors are widely expressed in a number of tissues and organs, possessing many regulatory functions related to cellular proliferation, differentiation, DNA repair, cell-cycle and cell apoptosis. E2F8 is a recently identified member of the E2F family with a duplicated DNA-binding domain feature discriminated from E2F1-6, controlling gene expression in a dimerization partner-independent manner. It is indispensable for angiogenesis, lymphangiogenesis and embryonic development. Although E2F8 and E2F7 perform complementary and overlapping functions in many cell metabolisms, E2F8, but not E2F7, overexpresses remarkably in hepatocellular carcinoma (HCC) to facilitate the HCC occurrence and development via activating a E2F1/ Cyclin D1 signaling pathway to regulate the G1- to S-phase transition of cell cycle progression or transcriptionally suppressing CDK1 to induce hepatocyte polyploidization. It also involves closely a variety of cellular physiological functions and pathological processes, which may bring a new breakthrough for the treatment of certain diseases, especially the HCC. Here, we summarize the latest progress of E2F8 on its relevant functions and mechanisms as well as potential application.

Keywords: E2F8, Hepatocellular carcinoma, angiogenesis, lymphangiogenesis, polyploidization, DNA damage.

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How to cite this article:
Lv Y, Xiao J, Liu J, Xing F. E2F8 is a Potential Therapeutic Target for Hepatocellular Carcinoma. J Cancer 2017; 8(7):1205-1213. doi:10.7150/jca.18255. Available from http://www.jcancer.org/v08p1205.htm