The Spectrum of E2F in Liver DiseaseMediated Regulation in Biology and Cancer

被引:9
|
作者
Huntington, Justin T. [1 ]
Tang, Xing [2 ,3 ,4 ]
Kent, Lindsey N. [2 ,3 ,4 ]
Schmidt, Carl R. [1 ]
Leone, Gustavo [2 ,3 ,4 ]
机构
[1] Ohio State Univ, Wexner Med Ctr, Dept Surg, Columbus, OH 43210 USA
[2] Ohio State Univ, Coll Med, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA
[3] Ohio State Univ, Coll Biol Sci, Dept Mol Genet, Columbus, OH 43210 USA
[4] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA
关键词
HUMAN HEPATOCELLULAR-CARCINOMA; CELL-CYCLE ARREST; GROWTH IN-VIVO; TRANSCRIPTION FACTORS; DOWN-REGULATION; GASTRIC-CANCER; CHEMOTHERAPEUTIC EFFICACY; HEPATIC STEATOSIS; MOUSE DEVELOPMENT; MAMMALIAN-CELLS;
D O I
10.1002/jcp.25242
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Uncoordinated cell growth is one of the fundamental concepts in carcinogenesis and occurs secondary to dysregulation of the cell cycle. The E2Fs are a large family of transcription factors and are key regulators of the cell cycle. The activation of E2Fs is intimately regulated by retinoblastoma 1 (RB1). The RB pathway has been implicated in almost every human malignancy. Recently there have been exciting developments in the E2F field using animal models to better understand the role of E2Fs in vivo. Genetic mouse models have proven essential in implicating E2Fs in hepatocellular carcinoma (HCC) and liver disease. In this review, the general structure and function of E2Fs as well as the role for E2Fs in the development of HCC and liver disease is evaluated. Specifically, what is known about E2Fs in human disease is explored in depth, and future directions are discussed. J. Cell. Physiol. 231: 1438-1449, 2016. (c) 2015 Wiley Periodicals, Inc.
引用
收藏
页码:1438 / 1449
页数:12
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