| Budget Amount *help |
¥16,640,000 (Direct Cost: ¥12,800,000、Indirect Cost: ¥3,840,000)
Fiscal Year 2017: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2015: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
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| 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.
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