2017 Fiscal Year Final Research Report
GPR30 signaling regulates Epithelial-Mesenchymal Transition in ovarian cancer
Project/Area Number |
15K10738
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Obstetrics and gynecology
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Research Institution | Osaka Medical College |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
林 正美 大阪医科大学, 医学部, 講師 (00551748)
大道 正英 大阪医科大学, 医学部, 教授 (10283764)
田中 良道 大阪医科大学, 医学部, 講師 (10625502)
金村 昌徳 大阪医科大学, 医学部, 非常勤講師 (40298782)
恒遠 啓示 大阪医科大学, 医学部, 講師 (70388255)
田辺 晃子 大阪医科大学, 医学部, 非常勤講師 (70454543)
佐々木 浩 大阪医科大学, 医学部, 助教 (80432491)
寺井 義人 大阪医科大学, 医学部, 准教授 (90278531)
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | 卵巣癌 / GPR30 / EMT |
Outline of Final Research Achievements |
The effect of GPR30 on EMT were evaluated in ovarian cancer cell line, A2780, which were cultured both in two-dimensional (2D) culture and three-dimensional (3D) culture model. GPR30 agonist, G1, was used to confirm the regulatory effects of GPR30 on the change of phenotypic modulation and EMT markers expression. In 3D culture, the stimulation of GPR30 leads the floating and sphere formation in A2780. G1-induced EMT was observed with related regulation of EMT markers expression at both mRNA and protein level. G1 induced the decrease of E-cadherin level and the increase of Snail and Vimentin in RT-PCR and Western blotting. Knockdown of GPR30, using siRNA, blocked G1-induced EMT. So, GPR30 might be an important molecule related to metastasis process in ovarian cancer.
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Free Research Field |
産婦人科
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