Elucidation of the new mechanism for breast carcinogenesis associated with early endosome.

2014 Fiscal Year Final Research Report

• Project/Area Number: 25640061
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: MIKI Yoshio 東京医科歯科大学, 難治疾患研究所, 教授 (10281594)
• Co-Investigator(Kenkyū-buntansha): NAKANISHI Akira 東京医科歯科大学, 難治疾患研究所, 准教授 (50321790)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 乳がん / BRCA2 / エンドサイトーシ / ESCRT複合体

Outline of Final Research Achievements

We already reported that BRCA2 is involved in the abscission between two daughter cells during cytokinesis. The event of membrane abscission also occurs during endosome formation, so we made hypothesis that BRCA2 might have some role in the event of endosome formation through membrane abscission. We isolated endosome lysates from HeLa S3 cells and analyzed the lysates by mass spectrometry or immunoblotting using anti-BRCA2 antibody. The results indicated that the BRCA2 localizes at early endosome. Furthermore, BRCA2 and GFP-Rab5, which was over expressed as a marker of early endosome, were showed the co-localization using immunofluorescence microscopy. However, the interaction of both proteins are still unclear from the immunoblotting data using total whole cell lysates. Then, we tried the mass spectrometry analysis of the anti-BRCA2 immunoprecipitates from endosome lysates. This results suggested the possibility of new BRCA2 function at early endosome.

Free Research Field

分子腫瘍学