2009 Fiscal Year Final Research Report
Studies on cytostatic antitumor mechanism by a new PI3K inhibitor ZSTK474
Project/Area Number |
20790087
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Biological pharmacy
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Research Institution | Japanese Foundation For Cancer Research |
Principal Investigator |
DAN Shingo Japanese Foundation For Cancer Research, 分子薬理部, 研究員 (70332202)
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Project Period (FY) |
2008 – 2009
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Keywords | PI3K / DNAチップ / 細胞周期 / アポトーシス / 抗がん剤 |
Research Abstract |
We demonstrated that PI3K inhibitors including ZSTK474 did not induce apoptosis but G_0/G_1 arrest of cell cycle in cancer cell lines with PIK3CA/PTEN aberrations in vitro. In parallel, PI3K inhibitors exhibited their antitumor effect without inducing apoptosis in vivo. We examined gene expression changes after treatment of cancer cells with ZSTK474 by using GeneChip, and found induction of CDK inhibitor p15 and repression of CDC25A after ZSTK474 treatment. These changes would be involved in G_0/G_1 arrest of cell cycle.
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Research Products
(18 results)
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[Journal Article] Correlating PI3K inhibitor efficacy with signaling pathway status: in silico and biological evaluations2010
Author(s)
Dan S, Okamura M, Seki M, Yamazaki K, Sugita H, Okui M, Mukai Y, Nishimura H, Asaka R, Nomura K, Ishikawa Y, Yamori T.
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Journal Title
Cancer Res. 70(12)
Pages: 4982-94
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