Mice lacking a transcriptional corepressor Tob are predisposed to cancer. Academic Article uri icon

Overview

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.

authors

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

publication date

  • May 15, 2003

Research

keywords

  • Carrier Proteins
  • Genetic Predisposition to Disease
  • Intracellular Signaling Peptides and Proteins
  • Neoplasms, Experimental
  • Transcription, Genetic
  • Tumor Suppressor Proteins

Identity

PubMed Central ID

  • PMC196063

Scopus Document Identifier

  • 0037948872

Digital Object Identifier (DOI)

  • 10.1101/gad.1088003

PubMed ID

  • 12756225

Additional Document Info

volume

  • 17

issue

  • 10