Pinpoint targeting of hepatocellular carcinoma for new therapeutic application
| Project/Area Number |
24501354
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Clinical oncology
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| Research Institution | Osaka City University |
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Principal Investigator |
KAKEHASHI Anna 大阪市立大学, 医学(系)研究科(研究院), 講師 (60382222)
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| Co-Investigator(Kenkyū-buntansha) |
WANIBUCHI Hideki 大阪市立大学, 医学(系)研究科(研究院), 教授 (90220970)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 分子標的治療 / 肝臓癌 / siRNA / ヌードマウス / 肝細胞癌 |
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| Outline of Final Research Achievements |
Knockdown (kn) of CNPY2 and CACHD1 in hepatocellular cancer cell lines was found to suppress their cell survival, proliferation and invasion activity. Inactivation of Nrf2, CEBPA, HNF1A and FOXA2 in CNPY2kn and CACHD1kn cells, and c-myc and N-myc in CACHD1kn cells was predicted. CNPY2 and CACHD1 knock-in of COS1 and COS7 cells elevated their cell proliferation and invasion activities likely to be due to activation of TGFbeta signaling. Systemic CNPY2 and CACHD1 knockdown in hepatocellular cancer xenografts nude mice models significantly suppressed the growth of tumors due to inhibition of cell proliferation and induction of tumor cellular apoptosis. These findings demonstrate that CNPY2 and CACHD1 knockdown can inhibit the growth of liver cancer xenografts. CNPY2 and CACHD1 might have a potential as new molecular therapeutic targets for human liver cancer.
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Report
(4 results)
Research Products
(21 results)
