The RASSF3 Candidate Tumor Suppressor Induces Apoptosis and G1–S Cell-Cycle Arrest via p53

DOI PDF PubMed 被引用文献6件 参考文献35件 オープンアクセス
  • Takumi Kudo
    Authors' Affiliations: Departments of 1Medical Biochemistry and 2Neurosurgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan; and 3Department of Ultrasound, Shengjing Hospital of China Medical University, Shenyang, China
  • Mitsunobu Ikeda
    Authors' Affiliations: Departments of 1Medical Biochemistry and 2Neurosurgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan; and 3Department of Ultrasound, Shengjing Hospital of China Medical University, Shenyang, China
  • Misa Nishikawa
    Authors' Affiliations: Departments of 1Medical Biochemistry and 2Neurosurgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan; and 3Department of Ultrasound, Shengjing Hospital of China Medical University, Shenyang, China
  • Zeyu Yang
    Authors' Affiliations: Departments of 1Medical Biochemistry and 2Neurosurgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan; and 3Department of Ultrasound, Shengjing Hospital of China Medical University, Shenyang, China
  • Kikuo Ohno
    Authors' Affiliations: Departments of 1Medical Biochemistry and 2Neurosurgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan; and 3Department of Ultrasound, Shengjing Hospital of China Medical University, Shenyang, China
  • Kentaro Nakagawa
    Authors' Affiliations: Departments of 1Medical Biochemistry and 2Neurosurgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan; and 3Department of Ultrasound, Shengjing Hospital of China Medical University, Shenyang, China
  • Yutaka Hata
    Authors' Affiliations: Departments of 1Medical Biochemistry and 2Neurosurgery, Graduate School of Medicine, Tokyo Medical and Dental University, Tokyo, Japan; and 3Department of Ultrasound, Shengjing Hospital of China Medical University, Shenyang, China

書誌事項

公開日
2012-05-31
資源種別
journal article
DOI
  • 10.1158/0008-5472.can-12-0572
公開者
American Association for Cancer Research (AACR)

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説明

<jats:title>Abstract</jats:title> <jats:p>RASSF3 is the smallest member of the RASSF family of proteins that function as tumor suppressors. Unlike other members of this important family, the mechanisms through which RASSF3 suppresses tumor formation remain unknown. Here, we show that RASSF3 expression induces p53-dependent apoptosis and its depletion attenuates DNA damage–induced apoptosis. We found that RASSF3-induced apoptosis depended upon p53 expression. Exogenous expression of RASSF3 induced G1–S arrest, which was also p53 dependent. In contrast, loss of RASSF3 promoted cell-cycle progression, abrogated UVB- and VP-16–induced G1–S arrest, decreased p53 protein and target gene expression, and prevented DNA repair. RASSF3 was shown to directly interact with and facilitate the ubiquitination of MDM2, the E3 ligase that targets p53 for degradation, thereby increasing p53 stabilization. Together, our findings show the tumor suppressor activity of RASSF3, which occurs through p53 stabilization and regulation of apoptosis and the cell cycle. Cancer Res; 72(11); 2901–11. ©2012 AACR.</jats:p>

収録刊行物

  • Cancer Research

    Cancer Research 72 (11), 2901-2911, 2012-05-31

    American Association for Cancer Research (AACR)

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