Knockdown of long non-coding RNA DDX11-AS1 inhibits the proliferation, migration and paclitaxel resistance of breast cancer cells by upregulating microRNA-497 expression

Abstract

Drug resistance is a major problem to overcome in the treatment of cancer; therefore, identifying therapeutic targets for drug resistance is a point of focus in the field of cancer research. Long non-coding RNAs (lncRNAs) and microRNAs (miRs) not only affect gene expression regulation during cell proliferation, but also have several potential roles in the drug resistance of malignant tumors. Reverse transcrip- tion-quantitative PCR was used to detect the expression levels of DDX11 antisense RNA 1 (DDX11-AS1) and miR-497 in MCF-7 and MDA-MB-231 cells. Cell transfection techniques were used to interfere with the expression levels of DDX11-AS1 and miR-497. Cell Counting Kit-8 and MTT assays were used to detect cell viability. A colony formation assay was used to detect cell proliferation. Wound-healing and Transwell assays were performed to measure the levels of cell migration and inva- sion. Western blotting was used to analyze the expression levels of migration-associated proteins, and immunofluorescence and western blotting were used to determine the expres- sion levels of the epithelial-mesenchymal transition-related proteins E-cadherin and N-cadherin, respectively. A luciferase reporter gene assay was used to verify the targeted binding of DDX11-AS1 and miR-497. The present study demonstrated that the expression levels of lncRNA DDX11-AS1 were mark- edly increased in paclitaxel (PTX)-resistant breast cancer cell lines. By contrast, knockdown of DDX11-AS1 expression inhibited PTX resistance of breast cancer cells, and suppressed the proliferation, invasion and migration of breast cancer cells, which was achieved via upregulation of miR-497 expression. In conclusion, knockdown of lncRNA DDX11-AS1 could inhibit the proliferation, migration and PTX resistance of breast cancer cells by upregulating miR-497 expression.