Effects of long noncoding RNA-ROR on tamoxifen resistance of breast cancer cells by regulating microRNA-205

Abstract

Purpose

To explore how long noncoding RNA-ROR (lncRNA-ROR) affects the tamoxifen resistance of breast cancer cells.

Methods

Breast epithelial (MCF10A), breast cancer (MCF7), and natural tamoxifen-resistant breast cancer (MDA-MB-231) cell lines were selected, and the relative lncRNA-ROR expressions were detected using quantitative real-time polymerase chain reaction (qRT-PCR). In vitro induction of TR5 cell line was performed. There were six groups: MCF7, MCF7/TR5, MDA-MB-231, MCF7-ROR, MCF7/TR5 ROR-siRNA, and the MDA-MB-231 ROR-siRNA groups. CCK-8 assay was conducted to assess the changes in drug resistance of each group. The expression of the epithelial mesenchymal transition (EMT) marker was detected using Western blotting. Transwell was selected to test the invasive ability of the cells. Expressions of microRNA-205 (miR-205) and ZEB1/2 were detected using qRT-PCR .

Results

Compared with the MCF7 cells, the proliferation rates of the MCF7/TR5 and MDA-MB-231 cells were significantly increased. Compared with the MCF7 cells, the MCF7-ROR cells had remarkably higher proliferation rates, down-regulated E-cadherin and miR-205 expressions, as well as increased vimentin, invasive ability, and mRNA expression of ZEB1 and ZEB2. Compared with the MCF7/TR5 and MDA-MB-231 cells, up-regulated E-cadherin and miR-205 expression, down-regulated expression of vimentin, ZEB1, and ZEB2 mRNA, and decreased invasive ability were observed in the MCF7/TR5 ROR-siRNA and MDA-MB-231 ROR-siRNA cells.

Conclusion

In MDA-MB-231 cells, down-regulated lncRNA-ROR could inhibit the EMT of breast cancer cells and enhance the sensibility of breast cancer cells to tamoxifen by increasing miR-205 expression and suppressing the expressions of ZEB1 and ZEB2.

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