Mice lacking a transcriptional corepressor Tob are predisposed to cancer
Mice lacking a transcriptional corepressor Tob are predisposed to cancer
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DOI：
10.1101/gad.1088003
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发表时间：
2003-05-15
影响因子：
10.5
通讯作者：
Yamamoto, T
中科院分区：
文献类型：
--
作者：
Yoshida, Y;Nakamura, T;Yamamoto, T
Tob是抗增殖家族基因的成员。缺乏tob的小鼠容易自发形成肿瘤。二乙基亚硝胺诱导的肝脏肿瘤在tob（-/-）小鼠中的发生率高于野生型小鼠。Tob (-/-)p53（-/-）小鼠的肿瘤形成速度比单阴性小鼠快。不含Tob时，cyclin D1 mRNA的表达增加，Tob降低cyclin D1 mRNA的表达。Tob作为转录辅抑制因子，通过与组蛋白去乙酰化酶的相互作用抑制cyclin D1启动子活性。在人类癌症中，tob mRNA的水平经常降低，这意味着tob与癌症的发展有关。
Tob is a member of antiproliferative family genes. Mice lacking tob are prone to spontaneous formation of tu-Mors. The occurrence rate of diethylnitrosamine-induced liver tumors is higher in tob(-/-) mice than in wildtype mice. tob(-/-)p53(-/-) mice show accelerated tumor formation in comparison with single null mice. Expression of cyclin D1 mRNA is increased in the absence of Tob and is reduced by Tob. Tob acts as a transcriptional corepressor and suppresses the cyclin D1 promoter activity through an interaction with histone deacetylase. Levels of tob mRNA are often decreased in human cancers, implicating tob in cancer development.