Analysis of cell death and repair pathway choice of DNA double-strand breaks caused by anti-cancer drug

2015 Fiscal Year Final Research Report

• Project/Area Number: 24710061
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Risk sciences of radiation/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, 先端科学研究指導者育成ユニット, 助教 (30707633)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: DNA二本鎖切断 / 非相同末端連結 / 相同組換え / カンプトテシン / ユビキチン

Outline of Final Research Achievements

DNA double-strand breaks (DSBs) are severe DNA damage that can be caused by anti-cancer drug to kill cancer cells. Camptothecin (CPT) causes DSB via DNA replication in growing cells. However, cellular responses to DNA replication-mediated DSB (RM-DSB) had not been revealed. In this study, we analyzed regulatory mechanisms of RM-DSB repair pathway and discovered that UbcH5c, a E2 ubiquitin-conjugating enzyme, is involved in NHEJ pathway of RM-DSB repair leading to chromosomal aberration.

Free Research Field

細胞生物学