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

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 transcription‑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 invasion. Western blotting was used to analyze the expression levels of migration‑associated proteins, and immunofluorescence and western blotting were used to determine the expression 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 markedly 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.