Development of a novel strategy for the elimination of cancer cell inactivated p53

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04305
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Tumor diagnostics
• Research Institution: National Cancer Center Japan
• Principal Investigator: Tsuchiya Naoto 国立研究開発法人国立がん研究センター, 研究所, ユニット長 (30322712)
• Research Collaborator: FUJIWARA Yuko 国立研究開発法人国立がん研究センター, 研究所・分子発がん研究ユニット, 非常勤研究員
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: p53 / microRNA / NEK9

Outline of Final Research Achievements

The p53 tumor-suppressor networks are crucial cellular components to prevent transformation of normal cells under exposure to various oncogenic insults. We previously identified NEK9 as an important cellular molecule that is required for the progression of cell cycle at G1 to S phase. NEK9 knockdown induced the inhibition of cell proliferation exclusively in p53 mutant and deficient cancer cell lines with cell cycle arrest at G1 phase. We tried to identify NEK9 interacting proteins in p53 mutant cancer cells and identified several translation initiation factors. Among them, knockdown of molecule X induced strong inhibition of cell proliferation dominantly in p53 mutant cancer cells. Our detailed study demonstrated that NEK9 and X complex regulates translation of a certain subset of mRNA, which are needed for the proliferation of p53 mutant cancer cell. We are now conducting further analyses to clarify the mechanism for the control of cell cycle specifically in p53 mutant cells.

Free Research Field

分子細胞生物学