Analysis of the mechanism of cell sensitivity against anti-cancer drug caused by ubiquitination-dependent DNA-PK activation

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K16127
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Risk sciences of radiation and chemicals
• Research Institution: Kanazawa Medical University
• Principal Investigator: SAKASAI Ryo 金沢医科大学, 医学部, 助教 (10549950)
• Research Collaborator: SHIBATA Atsushi 群馬大学, 大学院医学系研究科・大学院研究教育支援センター, 研究講師 (30707633)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: DNA二本鎖切断 / 非相同末端連結 / 相同組換え修復

Outline of Final Research Achievements

Anti-cancer drug camptothecin (CPT) causes DNA double-strand break (DSB) containing a single-DNA end that is referred to as one-ended DSB. Given that contribution of non-homologous end joining (NHEJ) to the repair of one-ended DSBs are considered to sensitize cells to CPT, it is important to reveal the mechanism of NHEJ contribution to the repair of one-ended DSBs for consideration of CPT efficacy in the chemotherapy.
Several researches suggested that UbcH5 is involved in the appearance of chromosome aberrations and CPT-resistance via NHEJ. SIAH1 was also identified as E3 ubiquitin ligase that is involved in NHEJ activation, but it has showed different phenotypes from UbcH5 so far.

Free Research Field

分子生物学