2016 Fiscal Year Final Research Report
Identification of a factor determining invasion and metastasis in non-small cell lung cancer and its therapeutic application based on comprehensive microRNA analysis
| Project/Area Number |
26461195
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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 |
Respiratory organ internal medicine
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| Research Institution | Jichi Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
ENDOU Shunsuke 自治医科大学, 医学部, 教授 (10245037)
ISHIKAWA Yuichi 癌研究会, 病理部, 部長 (80222975)
TSUBOCHI Hiroyoshi 自治医科大学, 医学部, 准教授 (50406055)
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| Research Collaborator |
WATANABE Yasutaka
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 肺癌 / EZH2 / siRNA / マイクロRNA / 網羅的発現解析 / miR-4448 |
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| Outline of Final Research Achievements |
High protein expressions of enhancer of zeste homolog 2 (EZH2) and the induction of epithelial-mesenchymal transition (EMT).were observed in most cases of small cell lung cancer (SCLC). EZH2 siRNA was transfected into SCLC cell lines, SBC3 and SBC5 cells with high EZH2 expression, consequently leading to the repression of EMT. Comprehensive microRNA (miRNA) expression analysis detected increased or decreased expressions of multiple miRNAs in SBC3 and SBC5 cells transfected with EZH2 siRNA. Of these miRNAs, miR-4448 that showed the most significant increase of expression was defined as a candidate miRNA for the target of EZH2.
Functional analyses for miR-4448 showed that along with EMT, cellular proliferative, invasive, and metastatic potentials were significantly repressed in SBC3 and SBC5 cells transfected with mimics of miR-4448, compared to those transfected with negative controls. EZH2 may serve as an oncogene that induces EMT through repressing miR-4448 expression and its function.
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| Free Research Field |
呼吸器腫瘍学
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