scholarly journals [Retracted] microRNA‑206 overexpression inhibits cellular proliferation and invasion of estrogen receptor α‑positive ovarian cancer cells

2021 ◽  
Vol 24 (3) ◽  
Author(s):  
Shaoru Li ◽  
Yan Li ◽  
Zhengfang Wen ◽  
Fanjing Kong ◽  
Xinlei Guan ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Cellular Proliferation ◽  
Estrogen Receptor Α ◽  
Ovarian Cancer Cells ◽  
Proliferation And Invasion

scholarly journals Differential induction of LRP16 by liganded and unliganded estrogen receptor α in SKOV3 ovarian carcinoma cells

2009 ◽  
Vol 202 (1) ◽  
pp. 167-177 ◽  
Author(s):  
Liyuan Tian ◽  
Zhiqiang Wu ◽  
Yali Zhao ◽  
Yuanguang Meng ◽  
Yiling Si ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Estrogen Receptor Α ◽  
Ovarian Cancer Cells ◽  
Induction Effect ◽  
Skov3 Cell ◽  
Signaling Transduction ◽  
Estrogen Response ◽  
Skov3 Cells

Previously, we investigated the induction effect of LRP16 expression by estrogen (17β-estradiol, E2) and established a feed-forward mechanism that activated estrogen receptor α (ERα) transactivation in estrogen-dependent epithelial cancer cells. LRP16 is required for ERα signaling transduction by functioning as an ERα coactivator. In this study, we demonstrated that LRP16 expression was upregulated in E2-responsive BG-1 ovarian cancer cells, but was downregulated in estrogen-resistant SKOV3 ovarian cancer cells. Pure estrogen antagonist ICI 182 780 did not affect LRP16 expression in SKOV3 cell. The unliganded ERα upregulated LRP16 expression and enhanced LRP16 promoter activity in SKOV3 cells; however, this induction was blocked by estrogen stimulation. Results from chromatin immunoprecipitation experiment revealed a strong recruitment of the unliganded ERα at LRP16 promoter in the absence of estrogen; however, ERα was largely released from the DNA upon E2 stimulation. Modulation in LRP16 expression level did not significantly change the proliferation rate of SKOV3 cells and the growth responsiveness of cells to E2. Knockdown of LRP16 by RNA interference in SKOV3 cells markedly attenuated estrogen response element-dependent ERα reporter gene activity and E2-induced c-Myc expression. Our study suggests a novel mechanism of estrogen resistance of ovarian cancer by which estrogen-repressed signaling pathway antagonizes estrogen-activated signaling transduction.

scholarly journals Activation of estrogen receptor α by estradiol and cisplatin induces platinum-resistance in ovarian cancer cells

2016 ◽  
Vol 18 (9) ◽  
pp. 730-739 ◽  
Author(s):  
Sohei Matsumura ◽  
Tsuyoshi Ohta ◽  
Keiko Yamanouchi ◽  
Zhiyang Liu ◽  
Takeshi Sudo ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Estrogen Receptor Α ◽  
Ovarian Cancer Cells ◽  
Platinum Resistance

scholarly journals Estrogen receptor β1 exerts antitumoral effects on SK-OV-3 ovarian cancer cells

2007 ◽  
Vol 193 (3) ◽  
pp. 421-433 ◽  
Author(s):  
Oliver Treeck ◽  
Georg Pfeiler ◽  
Diana Mitter ◽  
Claus Lattrich ◽  
Gerhard Piendl ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Cellular Proliferation ◽  
Kinase Inhibitor ◽  
Splice Variants ◽  
Ovarian Cancer Cell Line ◽  
Regulation Of Gene Expression ◽  
Ovarian Cancer Cells ◽  
Mrna Levels

Estrogen receptor (ER) β1 and its splice variants are expressed both in ovary and ovarian cancer. We studied the role of ERβ1 and two of its splice variants in regulation of gene expression, cellular proliferation, apoptosis, and migration of an ovarian cancer cell line. In this study, we transfected SK-OV-3 ovarian cancer cells with vectors coding for ERβ1 or its splice variants ERβ-δ125 and ERβ-δ1256, and tested their response to estrogen and tamoxifen in comparison with the untransfected cells. Heterologous expression of ERβ1, but not of the exon-deleted ERβ variants resulted in notably slower cell growth of SK-OV-3 ovarian cancer cells, an effect accompanied by more than tenfold increase of cyclin-dependent kinase inhibitor p21(WAF1) transcript levels and a significant reduction of cyclin A2 mRNA levels. SK-OV-3 cells stably overexpressing ERβ1 ligand independently also exhibited an increased apoptosis rate and a significantly decreased motility, an effect accompanied by upregulation of fibulin 1c. Our data demonstrate that ERβ1, but not the exon-deleted isoforms tested exerts multiple antitumoral effects on SK-OV-3 ovarian cancer cells even in the absence of estradiol or functional ERα.

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