| Project/Area Number |
21592149
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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
|
|---|
| Research Institution | Osaka Medical College |
|---|
Principal Investigator |
TANABE Akiko 大阪医科大学, 医学部, 助教 (70454543)
|
|---|
| 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)
KANEMURA Masanori 大阪医科大学, 医学部, 講師 (40298782)
SASAKI Hiroshi 大阪医科大学, 医学部, 助教 (80432491)
|
|---|
| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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)
|
|---|
| Keywords | 上皮性卵巣癌 / 抗癌剤耐性 / Akt-mTOR-HIF / VEGF / EMT / GPR30 / EGFR / CD24 / snail / E-cadherin / 白金製剤耐性卵巣癌 / 癌幹細胞 / 上皮間葉形質転換 |
|---|
| Research Abstract |
Epithelial-mesenchymal-transition(EMT) is recently identified as a important step in the invasion, metastasis, and chemo-resistance of cancer. We investigated whether topotecan increase the efficacy of cisplatin in in vitro and in vivo ovarian cancer models. Topotecan significantly inhibited the cisplatin-induced Akt activation, and regulated EMT-related factors in cisplatin-resistant ovarian cancer cell line. Furthermore, G protein-coupled receptor 30 is a 7-transmembrane estrogen receptor that functions alongside traditional estrogen receptors to regulate cellular responses to estrogen. In our studies suggested that GPR30 expression is linked to EMT phenotype, aggressive proliferation, and multiple drug resistance. Immunohistochemical examination revealed that expression of both GPR30 and EGFR contributes lower survival rates in epithelial ovarian cancer.
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