Cell cycle regulation of triple-negative breast cancer by newly-identified nuclear protein network.

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K07449
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 49020:Human pathology-related
• Research Institution: Aichi Medical University
• Principal Investigator: Kasai Kenji 愛知医科大学, 医学部, 教授 (70242857)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 乳癌 / トリプルネガティブ乳癌 / FAM64A / DNA修復機構

Outline of Final Research Achievements

FAM64A protein was found to be increased in the G2/M-phase of cell cycle. Knockdown of FAM64A in the TNBC cell lines showed the increase ofγH2AX and reduced the cell number, indicating FAM64A could be a therapeutic target at least in the FAM64A-positive TNBC cases. Pull-down assay of FAM64A-associated proteins followed by mass analysis identified a member of SWI/SNF factors that play a crucial role of DNA replication and repair. These evidence support the possibility that FAM64A is involved in the proper progression of the cell cycle in FAM64A-positive TNBC.

Free Research Field

分子病理学

Academic Significance and Societal Importance of the Research Achievements

本研究では約47%のトリプルネガティブ乳癌（TNBC）に発現している核蛋白FAM64Aから見たTNBCの細胞増殖特性と新規治療戦略のための基盤的知見を得ることを目的とした。FAM64A高発現TNBC細胞株でsiRNA法によりFAM64Aを欠損させると、DNA損傷マーカーγH2AXが増加し細胞数が減少した。このことから、FAM64A高発現TNBCではFAM64Aが治療標的になり得ることが示唆された。