拮抗小 DNA 肿瘤病毒转化蛋白的致癌活性。
Opposing oncogenic activities of small DNA tumor virus transforming proteins.
机构信息
Institute for Molecular Virology, Doisy Research Center, Saint Louis University Medical School, 1100 South Grand Blvd., 6th Floor, St. Louis, MO 63104, USA.
出版信息
Trends Microbiol. 2011 Apr;19(4):174-83. doi: 10.1016/j.tim.2011.01.003. Epub 2011 Feb 15.
Abstract
The E1A gene of species C human adenovirus is an intensely investigated model viral oncogene that immortalizes primary cells and mediates oncogenic cell transformation in cooperation with other viral or cellular oncogenes. Investigations using E1A proteins have illuminated important paradigms in cell proliferation and about the functions of cellular proteins such as the retinoblastoma protein. Studies with E1A have led to the unexpected discovery that E1A also suppresses cell transformation and oncogenesis. Here, I review our current understanding of the transforming and tumor-suppressive functions of E1A, and how E1A studies led to the discovery of a related tumor-suppressive function in benign human papillomaviruses. The potential role of these opposing functions in viral replication in epithelial cells is also discussed.
摘要
C 型人腺病毒的 E1A 基因是一种备受关注的病毒癌基因模型，它能使原代细胞永生化，并与其他病毒或细胞癌基因协同介导致癌细胞转化。使用 E1A 蛋白进行的研究阐明了细胞增殖的重要范例，以及视网膜母细胞瘤蛋白等细胞蛋白的功能。E1A 的研究导致了一个意外的发现，即 E1A 也能抑制细胞转化和致癌作用。在这里，我回顾了我们目前对 E1A 的转化和肿瘤抑制功能的理解，以及 E1A 研究如何导致在良性人乳头瘤病毒中发现相关的肿瘤抑制功能。还讨论了这些相反功能在上皮细胞中病毒复制中的潜在作用。
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