Analysis of cell death regulation by Prohibitin and Hint2 under hypoxia

• Project/Area Number: 24501312
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Tumor biology
• Research Institution: Keio University (2013-2014); The University of Tokyo (2012)
• Principal Investigator: SATOH Kiyotoshi 慶應義塾大学, 政策・メディア研究科, 助教 (50401386)
• Co-Investigator(Kenkyū-buntansha): KUBOTA Shunichiro 帝京平成大学, 薬学部, 教授 (00260480)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Project Status: Completed (Fiscal Year 2014)
• Budget Amount: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000); Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000); Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000); Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
• Keywords: 細胞死 / 低酸素 / 癌 / 癌細胞 / 細胞生存 / ＰＨＢ / 国際情報交換 / 多国籍

Outline of Final Research Achievements

Cancer cells are more resistant to hypoxia than normal cells. We found that mitochondrial protein Prohibitin was decreased under hypoxic conditions, and that overexpression of Prohibitin inhibited cell death induced by hypoxia. Furthermore, Knockdown of Prohibitin in human colon cancer cells reduced S phase cell fraction and decreased cell proliferation. In addition, we analyzed functional cooperation of Prohibitin and mitochondrial protein Hint2 in colon cancer cells.