| Project/Area Number |
17K16833
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Obstetrics and gynecology
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
HIROTA Yasushi
|
|---|
| Project Period (FY) |
2017-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 子宮内膜 / プロゲステロン / 細胞増殖 / 細胞分化 / 子宮 / マウスモデル / RB / 子宮内膜上皮 / 黄体ホルモン / 子宮体癌 / 着床 / MPA / RNA-seq / プロゲステロン受容体 |
|---|
| Outline of Final Research Achievements |
In association with progesterone (P4) resistance in endometrial cancer, we investigated cell proliferation of the endometrium stimulated by P4. Retinoblastoma protein (RB), which inhibits cell proliferation, was deleted in the mouse uterus using uterine specific RB conditional knockout mice. We found that RB and P4 cooperatively controls endometrial epithelial cell growth and embryo implantation, and cessation of cell proliferation in the endometrial epithelium is functionally important. We also found that P4 plays a role in the endometrial control of various signaling pathways associated with cell cycle regulation.
|
| Academic Significance and Societal Importance of the Research Achievements |
本研究により、P4による正常子宮内膜の細胞増殖抑制が子宮機能に与える意義が明確になった。子宮体癌の前がん病変ともいえる子宮内膜増殖症は不妊症の病歴を伴うことがしばしばであり、子宮内膜上皮の分化異常ともいえる状態であることが着床の妨げになっている可能性が考えられる。本研究により、P4による正常な子宮内膜の応答性とその異常の病態を理解する端緒になるため、究極的には子宮体癌におけるP4応答性の異常の理解に繋がるものと考える。
|
