International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


POSTER 163 - RIT1 TUMOR SUPPRESSOR GENE ISOLATED BY POSITIONAL CLONING SUPPRESSES TUMOR CELL GROWTH

Prof Ryo Kominami
Niigata University
asahimachi 1-757
Niigata
951-8510
Japan

Co-Authors: Wakabayashi Y, Inoue J, Matsuki A, Takahashi Y, Okano H, Mishima Y, Niwa o
Institutions: Kyoto University, Radiation Biology Center

Rit1 tumor suppressor gene isolated by positional cloning suppresses tumor cell growth.

Mouse genetic systems offer a number of useful features for positional cloning. However, no success was reported of tumor suppressor genes. We previously reported the isolation of a novel candidate tumor suppressor gene, Rit1, involved in g-ray induced mouse thymic lymphomas through genetic and physical mapping followed by sequence analysis. Bi-allelic alteration of Rit1 found in the lymphomas at a high frequency is fully consistent with the paradigm of the two-hit recessive model of oncogenesis. Here we show the ability of Rit1 proteins to suppress tumor cell growth and this has established Rit1 as a tumor suppressor gene. Introduction of Rit1 into Hela cells lacking Rit1 expression suppressed cell growth by colony formation and proliferation assays, and flow cytomeric analysis of the Rit1-inducible cell lines showed that the suppressin was mediated through increased apoptosis and did not involve cell cycle arrest. Since normal T-cell precursors in thymus and some T-cell lines express Rit1, expression of Rit1 proteins per se is not sufficient to induce apoptosis or suppress cell growth. Of interest, subcellular localization of Rit1 proteins was cytoplasmic in endogenously expressing MOLT4 T-cells but nuclear in Hela cells transfected with Rit1 clones. Hence the localization may be a key element for apoptosis given by Rit1, although the mechanism cont


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