Function of the novel tumor suppressor in cell division and carcinogenesis

2015 Fiscal Year Final Research Report

• Project/Area Number: 24300327
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Tumor biology
• Research Institution: Tohoku University
• Principal Investigator: Chiba Natsuko 東北大学, 加齢医学研究所, 教授 (50361192)
• Co-Investigator(Kenkyū-buntansha): WATABANE Toshio 奈良女子大学, 大学院人間文化研究科, 教授 (60201208)
• Co-Investigator(Renkei-kenkyūsha): KANNO Shin-ichiro 東北大学, 加齢医学研究所, 講師 (10400417) ; Sugimoto Asako 東北大学, 生命科学研究科, 教授 (80281715)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: BRCA1 / 中心体

Outline of Final Research Achievements

The breast and ovarian cancer specific tumor suppressor BRCA1 plays important roles in DNA repair and centrosome regulation. We identified Obg-like ATPase 1 (OLA1) that interacts with BRCA1. OLA1 directly bound to BRCA1 and a component of centrosome. OLA1 localized to centrosomes in interphase and to the spindle pole in mitotic phase, and its knockdown resulted centrosome amplification and the activation of microtubule aster formation. OLA1 with a mutation observed in breast cancer cell line failed to bind BRCA1 and rescue the OLA1 knockdown-induced centrosome amplification. BRCA1 variant found in familial breast cancer also abrogated the binding of BRCA1 to OLA1. These findings suggest that OLA1 plays an important role in centrosome regulation together with BRCA1.

Free Research Field

腫瘍生物学