| Project/Area Number |
16K19458
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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 |
Respiratory organ internal medicine
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| Research Institution | Kagoshima University |
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Principal Investigator |
MATAKI Hiroko 鹿児島大学, 附属病院, 医員 (60750750)
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| Co-Investigator(Renkei-kenkyūsha) |
Seki Naohiko 千葉大学, 大学院医学研究院, 准教授 (50345013)
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| Research Collaborator |
Inoue Hiromasa 鹿児島大学, 医歯学域医学系, 教授 (30264039)
Mizuno Keiko 鹿児島大学, 医歯学域医学系, 助教 (50531414)
Kumamoto Tomohiro 鹿児島大学, 附属病院, 特任助教 (20622517)
Kamikawaji Kazuto 鹿児島大学, 附属病院, 医員 (80633396)
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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 |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | microRNA / 肺癌 / 特発性肺線維症 / 核酸 / マイクロRNA / 肺線維症 |
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| Outline of Final Research Achievements |
Idiopathic pulmonary fibrosis (IPF) is frequently associated with lung cancer. However, the curative treatment has not been developed for the disease. We investigated novel RNA networks mediated by miRNAs, and identified the molecular targets involved in the pathology of the disease.
We confirmed the downregulation of miR-29a in clinical specimens of IPF and lung cancer. Restoration of miR-29a suppressed cancer cell aggressiveness and fibroblast migration. A combination of gene expression data and in silico analysis showed that lysyl oxidase-like 2 (LOXL2) and serpin peptidase inhibitor clade H, member 1 (SERPINH1) were direct targets of miR-29a, suggesting that these genes are involved in the pathogenesis of these two diseases.
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