Molecular mechanism of anti-mitogenic effects of estrogen on breast cancer cells
| Project/Area Number |
26462518
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
ISHIDA Maho 山梨大学, 大学院総合研究部, 助教 (80362086)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | エストロジェン / エストロジェン受容体 / MDA-MB-231 / 細胞増殖 / 増殖抑制 |
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| Outline of Final Research Achievements |
MDA-MB-231 is an estrogen receptor (ER)-negative breast cancer cell line. In contrast to the mitogenic effects of 17beta-estradiol (E2) in ER-positive MCF7, E2 suppresses proliferation of MDA-MB-231 stably transfected with ERalpha cDNA (MDA-ER). In MDA-ER, the BCAR3 and FOSL1 gene expressions were found to be suppressed by the treatment with E2. Because the knock-down of those gene expressions using RNA interference caused the inhibition of the proliferation of MDA-ER treated with vehicle, we hypothesized that the suppression of those gene expressions may be involved in the anti-mitogenic effects of E2. The overexpression of those genes, however, had no effect on the anti-mitogenic effects of E2. These results indicate that E2-induced down regulation of BCAR3 or FOSL1 gene expression does not play a key role for the anti-mitogenic effects of E2.
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Report
(5 results)
Research Products
(9 results)
