TRIM29 negatively regulates p53 via inhibition of Tip60 |
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Authors: | Takuya Sho Tadasuke TsukiyamaTomonobu Sato Takeshi KondoJun Cheng Takashi SakuMasahiro Asaka Shigetsugu Hatakeyama |
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Affiliation: | a Department of Biochemistry, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japanb Department of Gastroenterology and Hematology, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido 060-8638, Japanc Division of Oral Pathology, Department of Tissue Regeneration and Reconstruction, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8514, Japan |
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Abstract: | Ataxia-telangiectasia (AT) is an autosomal recessive genetic disease characterized by immunological deficiencies, neurological degeneration, developmental abnormalities and an increased risk of cancer. Ataxia-telangiectasia group D (ATDC) was initially described as a gene related to AT. Ataxia-telangiectasia group D, also known as TRIM29, is structurally a member of the tripartite motif (TRIM) family of proteins, some of which have been reported to be highly expressed in some human carcinomas, but the involvement of TRIM29 in carcinogenesis has not been fully elucidated. In this study, we found by using yeast two-hybrid screening that TRIM29 binds to Tip60, which has been reported as a cellular acetyltransferase protein. Overexpression of TRIM29 promoted degradation and changed localization of Tip60 and reduced acetylation of p53 at lysine 120 by Tip60, resulting in enhancement of cell growth and transforming activity. In addition, we found that TRIM29 suppresses apoptosis induced by UV irradiation in HCT116 cell lines. These findings suggest that TRIM29 functions as an oncogene that promotes tumor growth. |
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Keywords: | TRIM29 p53 Tip60 Ubiquitin Ataxia-telangiectasia |
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