Mechanism for cancer-related upregulation of the Rad54B-mediated cellular function network

2016 Fiscal Year Final Research Report

• Project/Area Number: 15H06146
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Single-year Grants
• Research Field: Tumor biology
• Research Institution: The University of Tokyo
• Principal Investigator: YASUHARA Takaaki 東京大学, 大学院医学系研究科(医学部), 助教 (90757056)
• Project Period (FY): 2015-08-28 – 2017-03-31
• Keywords: がん / 細胞機能ネットワーク / Rad54B / 細胞周期 / E2Fファミリー

Outline of Final Research Achievements

We have previously shown that Rad54B, by interacting with various proteins, forms a network that links among the cellular functions. In clinical cancer samples, constitutive upregulation of Rad54B is frequently observed and associated with poor prognosis, suggesting that the Rad54B-mediated cellular function network is involved in the neoplastic process. In this study, we aimed to reveal how Rad54B expression is controlled, and found that the Rad54B expression is regulated in a cell cycle-dependent manner. Mechanistically, the E2F family, a set of transcription factors for cell cycle-regulated genes, binds to the Rad54B promoter region to upregulate the Rad54B expression in S/G2 phase and to downregulate that in G0/G1 phase. Taken together with our previous findings that Rad54B regulates the cell cycle machinery, these data suggest the existence of a mutual regulatory mechanism between the Rad54B-mediated cellular function network and cell cycle machinery.

Free Research Field

がん細胞生物学