E2F8 is a Potential Therapeutic Target for Hepatocellular Carcinoma

被引:36
|
作者
Lv, Yi [1 ,2 ]
Xiao, Jia [1 ]
Liu, Jing [3 ]
Xing, Feiyue [1 ,2 ]
机构
[1] Jinan Univ, Inst Tissue Transplantat & Immunol, Dept Immunobiol, Guangzhou, Guangdong, Peoples R China
[2] Jinan Univ, Higher Educ Inst, Key Lab Funct Prot Res Guangdong, Guangzhou, Guangdong, Peoples R China
[3] Jinan Univ, Dept Stomatol, Guangzhou, Guangdong, Peoples R China
来源
JOURNAL OF CANCER | 2017年 / 8卷 / 07期
基金
中国国家自然科学基金;
关键词
E2F8; Hepatocellular carcinoma; angiogenesis; lymphangiogenesis; polyploidization; DNA damage; TRANSCRIPTION FACTOR FAMILY; DNA-REPLICATION; CELL; ANGIOGENESIS; VEGF; POLYPLOIDIZATION; EXPRESSION; CANCER; GROWTH; MEMBER;
D O I
10.7150/jca.18255
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:1205 / 1213
页数:9
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