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.

scholarly journals Effect of estrogen receptor β agonists on proliferation and gene expression of ovarian cancer cells

BMC Cancer ◽  
2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Susanne Schüler-Toprak ◽  
Christoph Moehle ◽  
Maciej Skrzypczak ◽  
Olaf Ortmann ◽  
Oliver Treeck
Keyword(s):  
Gene Expression ◽  
Ovarian Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Estrogen Receptor Β ◽  
Ovarian Cancer Cells

Bile acids upregulate BRCA1 and downregulate estrogen receptor 1 gene expression in ovarian cancer cells

2018 ◽  
Vol 27 (6) ◽  
pp. 553-556 ◽  
Author(s):  
Qunyan Jin ◽  
Olivier Noel ◽  
Mai Nguyen ◽  
Lionel Sam ◽  
Glenn S. Gerhard
Keyword(s):  
Gene Expression ◽  
Ovarian Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Bile Acids ◽  
Ovarian Cancer Cells ◽  
Estrogen Receptor 1

scholarly journals The Effect of 3′-Hydroxy-3,4,5,4′-Tetramethoxy -stilbene, the Metabolite of the Resveratrol Analogue DMU-212, on the Motility and Proliferation of Ovarian Cancer Cells

2020 ◽  
Vol 21 (3) ◽  
pp. 1100 ◽  
Author(s):  
Andrzej Nowicki ◽  
Paulina Skupin-Mrugalska ◽  
Malgorzata Jozkowiak ◽  
Marcin Wierzchowski ◽  
Marcin Rucinski ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cell Motility ◽  
Cancer Cells ◽  
Ovarian Cancer Cell Line ◽  
Parent Compound ◽  
Cancer Cell Line ◽  
Ovarian Cancer Cells ◽  
Published Data ◽  
Proliferative Effect ◽  
Tumor Cell Motility

Targeting tumor cell motility and proliferation is an extremely important challenge in the prevention of metastasis and improving the effectiveness of cancer treatment. We recently published data revealing that DMU-214, the metabolite of firmly cytotoxic resveratrol analogue DMU-212, exerted significantly higher biological activity than the parent compound in ovarian cancer cells. The aim of the present study was to assess the molecular mechanism of the potential anti-migration and anti-proliferative effect of DMU-214 in ovarian cancer cell line SKOV-3. We showed that DMU-214 reduced the migratory capacity of SKOV-3 cells. The microarray analysis indicated ontology groups of genes involved in processes of negative regulation of cell motility and proliferation. Furthermore, we found DMU-214 triggered changes in expression of several migration- and proliferation-related genes (SMAD7, THBS1, IGFBP3, KLF4, Il6, ILA, SOX4, IL15, SRF, RGCC, GPR56) and proteins (GPR56, RGCC, SRF, SMAD7, THBS1), which have been shown to interact to each other to reduce cell proliferation and motility. Our study showed for the first time that DMU-214 displayed anti-migratory and anti-proliferative activity in SKOV-3 ovarian cancer cells. On the basis of whole transcriptome analysis of these cells, we provide new insight into the role of DMU-214 in inhibition of processes related to metastasis.

scholarly journals Forkhead Box Protein C2 Promotes Epithelial-Mesenchymal Transition, Migration and Invasion in Cisplatin-Resistant Human Ovarian Cancer Cell Line (SKOV3/CDDP)

2016 ◽  
Vol 39 (3) ◽  
pp. 1098-1110 ◽  
Author(s):  
Chanjuan Li ◽  
Hongjuan Ding ◽  
Jing Tian ◽  
Lili Wu ◽  
Yun Wang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Epithelial Mesenchymal Transition ◽  
Ovarian Cancer Cell Line ◽  
Cancer Cell Line ◽  
Ovarian Cancer Cells ◽  
Skov3 Cell ◽  
Mesenchymal Transition ◽  
Forkhead Box

Background/Aims: Forkhead Box Protein C2 (FOXC2) has been reported to be overexpressed in a variety of human cancers. However, it is unclear whether FOXC2 regulates epithelial-mesenchymal transition (EMT) in CDDP-resistant ovarian cancer cells. The aim of this study is to investigate the effects of FOXC2 on EMT and invasive characteristics of CDDP-resistant ovarian cancer cells and the underlying molecular mechanism. Methods: MTT, Western blot, scratch wound healing, matrigel transwell invasion, attachment and detachment assays were performed to detect half maximal inhibitory concentration (IC50) of CDDP, expression of EMT-related proteins and invasive characteristics in CDDP-resistant ovarian cancer cell line (SKOV3/CDDP) and its parental cell line (SKOV3). Small hairpin RNA (shRNA) was used to knockdown FOXC2 and analyze the effect of FOXC2 knockdown on EMT and invasive characteristics of SKOV3/CDDP cells. Also, the effect of FOXC2 upregulation on EMT and invasive characteristics of SKOV3 cells was analyzed. Furthermore, the molecular mechanism underlying FOXC2-regulating EMT in ovarian cancer cells was determined. Results: Compared with parental SKOV3 cell line, SKOV3/CDDP showed higher IC50 of CDDP (43.26μM) (P<0.01) and acquired EMT phenotype and invasive characteristics. Gain- and loss-of-function assays indicated that shRNA-mediated FOXC2 knockdown could reverse EMT and reduce the capacity of migration, invasion, attachment and detachment in SKOV3/CDDP cell line and upregulation of FOXC2 could induce the reverse effects in parental SKOV3 cell line. Furthermore, it was found that activation of ERK or AKT/GSK-3β signaling pathways was involved in FOXC2-promoting EMT in CDDP-resistant ovarian cancer cells. Conclusions: Taken together, these data demonstrate that FOXC2 may be a promoter of EMT phenotype in CDDP-resistant ovarian cancer cells and a potential therapeutic target for the treatment of advanced ovarian cancer.

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