Mice lacking a transcriptional corepressor Tob are predisposed to cancer

Yutaka Yoshida, Takahisa Nakamura, Masato Komoda, Hitoshi Satoh, Toru Suzuki, Junko K. Tsuzuku, Takashi Miyasaka, Eri H. Yoshida, Hisashi Umemori, Reiko K. Kunisaki, Kenzaburo Tani, Shunsuke Ishii, Shigeo Mori, Masami Suganuma, Tetsuo Noda, Tadashi Yamamoto

Research output: Contribution to journalArticlepeer-review

93 Citations (Scopus)

Abstract

tob is a member of antiproliferative family genes. Mice lacking tob are prone to spontaneous formation of tumors. The occurrence rate of diethylnitrosamine-induced liver tumors is higher in tob-/- mice than in wild-type 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.

Original languageEnglish
Pages (from-to)1201-1206
Number of pages6
JournalGenes and Development
Volume17
Issue number10
DOIs
Publication statusPublished - 2003 May 15

Keywords

  • Corepressor
  • Liver cancer
  • Tob
  • cyclin D1 expression

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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