| Project/Area Number |
16K19349
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Gastroenterology
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| Research Institution | Ehime University |
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Principal Investigator |
Watanabe Takao 愛媛大学, 医学部附属病院, 講師 (90650458)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | PKR / hepatocellular carcinoma / DNA methylation / PKR inhibitor / proliferation / HCV / 肝細胞癌 / メチル化 / C型肝炎ウイルス / 治療標的 / イメージング |
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| Outline of Final Research Achievements |
Double-stranded RNA-activated protein kinase R (PKR) is upregulated by hepatitis C virus (HCV), and also overexpressed in hepatocellular carcinoma (HCC) with HCV infection. In HCC cell line Huh 7, we elucidated PKR inhibitor administration significantly decrease tumor cell proliferation in a dose dependent manner by in vitro proliferation assay. To evaluate the tumor suppressive effect of PKR inhibitor in vivo, we inoculated Huh 7 cells subcutaneously into BALB/c-nu/nu mice. The mice were then injected i.p. every day with or without PKR inhibitor. Then PKR inhibitor suppressed the proliferation of HCC cells in a dose dependent manner. Moreover we identified DNA methylation level of several cancer related genes were changed by PKR-knockdown in HCV infected HCC cells using the human Methylation450 BeadChipTM. PKR promotes the proliferation of HCC cells, and PKR inhibitor could serve as an attractive therapeutic approach.
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