Molecular mechanism of anti-mitogenic effects of estrogen on breast cancer cells

2017 Fiscal Year Final Research Report

• Project/Area Number: 26462518
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: University of Yamanashi
• Principal Investigator: ISHIDA Maho 山梨大学, 大学院総合研究部, 助教 (80362086)
• Project Period (FY): 2014-04-01 – 2018-03-31
• 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

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.

Free Research Field

医歯薬学