Project/Area Number |
15K15604
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Obstetrics and gynecology
|
Research Institution | Nagoya University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
SENGA Takeshi 名古屋大学, 大学院医学系研究科, 准教授 (80419431)
|
Project Period (FY) |
2015-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 卵巣癌 / 腹膜播種 / 腹膜中皮細胞 / 腹膜間隙透過性 / filopodia形成 / 細胞コミュニケーション / アクチンモーター蛋白 / 浸潤 |
Outline of Final Research Achievements |
Epithelial ovarian carcinoma (EOC) is believed to cause peritoneum dissemination through microenvironmental cell-to-cell communication between the tumor and mesothelium, leading to the further acquisition of progressive and metastatic potentials. In the present study, we aimed to determine the role of cancer-associated mesothelial cells (CAMCs) in the maintenance of cisplatin-resistance. Normal mesothelium (MC) showed an epithelial morphology with a cobblestone appearance. When MCs were co-cultured with malignant ascites from patients with advanced EOC, a dramatic morphologic change was noted from an epithelioid pattern to a-SMA-positive fibroblastic, mesenchymal pattern. Our findings indicate the possible involvement of CAMCs in the maintenance of cisplatin-resistance, resulting in being “seeds of recurrence”. The novel mechanism of CAMCs as a facilitator of EOC progression is displayed through microenvironmental cell-to-cell communication between EOC and the mesothelium.
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