E2F8 Contributes to Human Hepatocellular Carcinoma via Regulating Cell Proliferation
E2F8 Contributes to Human Hepatocellular Carcinoma via Regulating Cell Proliferation
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E2F8 通过调节细胞增殖促进人类肝细胞癌
DOI：
10.1158/0008-5472.can-09-3082
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发表时间：
2010-01-15
期刊：
影响因子：
11.2
通讯作者：
Han, Ze-Guang
中科院分区：
文献类型：
--
作者：
Deng, Qing;Wang, Qun;Han, Ze-Guang
转录因子的E2 F家族成员包括非典型成员E2 F8，其在癌症中的研究很少。我们报告说，E2 F8是强烈上调，在人类肝细胞癌（HCC），它被证明有助于肿瘤的发生和发展。E2 F8的异位过表达促进细胞增殖、集落形成和致瘤性，而E2 F8敲低抑制这些表型，如Huh-7、Focus、Hep 3B和YY-8103 HCC细胞系中所记录的。机制分析表明，E2 F8可以与cyclin D1的调控元件结合，调节其转录，促进S期细胞的积累。总之，我们的研究结果表明，E2 F8有助于肝癌的致癌潜力，并可能构成这种疾病的潜在治疗靶点。Cancer Res; 70（2）; 782-91.（C）2010年AACR。
The E2F family member of transcription factors includes the atypical member E2F8, which has been little studied in cancer. We report that E2F8 is strongly upregulated in human hepatocellular carcinoma (HCC), where it was evidenced to contribute to oncogenesis and progression. Ectopic overexpression of E2F8 promoted cell proliferation, colony formation, and tumorigenicity, whereas E2F8 knockdown inhibited these phenotypes, as documented in Huh-7, Focus, Hep3B, and YY-8103 HCC cell lines. Mechanistic analyses indicated that E2F8 could bind to regulatory elements of cyclin D1, regulating its transcription and promoting accumulation of S-phase cells. Together, our findings suggest that E2F8 contributes to the oncogenic potential of HCC and may constitute a potential therapeutic target in this disease. Cancer Res; 70(2); 782-91. (C)2010 AACR.