| Project/Area Number |
21592148
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Osaka Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
OHMICHI Masahide 大阪医科大学, 医学部, 教授 (10283764)
TERAI Yoshito 大阪医科大学, 医学部, 講師 (90278531)
TANABE Akiko 大阪医科大学, 医学部, 助教 (70454543)
SASAKI Hiroshi 大阪医科大学, 医学部, 助教 (80432491)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 子宮内膜癌 / GPR30 / 上皮間葉形質転換 / snail / slug / E-cadherin / CD24 / プロゲステロン受容体 |
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| Research Abstract |
The aims of our study were to evaluate the role of MPA for the regulation of tumor progression. In type 1 endometrial cancer cell line, MPA did not activate both ERK and Akt, However, ERK and Akt were phosphorylated by MPA in type 2 cell line. Interestingly, estradiol(E2) activated ERK and Akt in both cell lines. Therefore, GPR30, a membrane receptor for E2, might be a key molecule for tumor progression in both type 1 and type 2 endometrial cancers. The activation of GPR30 was associated to tumor proliferation via up regulation of cyclin D1.Furthermore, epithelial-mesenchymal-transition(EMT) is recently identified as an important step in the invasion and metastasis of cancer. Our data indicate that reduced E-cadherin and nuclear expression of Snail and Slug have a prognostic impact in endometrial cancer. Therefore, to clarify and control of EMT signaling is a promising molecular targeting therapy in endometrial cancer.
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