| Project/Area Number |
26861073
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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 |
Digestive surgery
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| Research Institution | Osaka University |
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Principal Investigator |
Tomihara Hideo 大阪大学, 医学部附属病院, 医員 (30724231)
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| Co-Investigator(Kenkyū-buntansha) |
Nagano Hiroaki 大阪大学, 医学(系)研究科(研究院), 准教授 (10294050)
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| Co-Investigator(Renkei-kenkyūsha) |
Kobayashi Shogo 大阪大学, 医学(系)研究科(研究院), 助教 (30452436)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | リプログラミング / miR-302 / LSD1 / ヒストン脱アセチル化 / miRNA |
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| Outline of Final Research Achievements |
We have reported two original issues; 1. Applying the conventional reprograming technology for cancer cells attenuated malignant potentials including the resistance ability to anti-cancer drugs. 2. An induction of several microRNAs including miR-302, can reprogram somatic cells as well as the conventional reprograming technology. Since the change were reversible, microRNA-induced reprograming procedure may include certain epigenetic mechanisms. To reveal the mechanisms, we investigated the hepatocellular carcinoma cells reprogrammed with miR-302 transduction. We found that the suppression of LSD1, which was one of the target genes of miR-302, increased anti-cancer drug sensitivities through the suppression of deacetylations of Histone H3-K4 and introduced them to an apoptosis. Taken together these results, LSD1 inhibitor could be a new therapeutic option for anti-cancer therapy.
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