Abstract
Breast cancer has become the most common female tumor in the world. Although great progress has been made in the past decade, the treatment of advanced breast cancer remains unsatisfactory. An increasing number of reports have indicated that long non-coding RNAs (lncRNAs) have a pivotal role in chemoresistance as potential oncogenes in numerous types of cancer. However, the precise mechanisms underlying the action of lncRNAs in breast cancer resistance to chemotherapy have yet to be fully elucidated. In the present study, the function and molecular mechanisms of the lncRNA TMPO-antisense RNA 1 (AS1) in terms of its resistance to docetaxel (DOC) were explored in the MDA-MB-231 and MCF7 breast cancer cell lines. The results obtained suggested that TMPO-AS1 was markedly upregulated in DOC-resistant breast cancer cells compared with the sensitive breast cancer cells. Functionally, TMPO-AS1-knockdown sensitized MDA-231/DOC and MCF-7/DOC cells to DOC and suppressed cell invasion, with increased rates of DOC-induced apoptosis. Mechanistically, TMPO-AS1-downregulation induced DOC-sensitivity in breast cancer cells via depleting tripartite motif-containing protein 37 (TRIM37) by sponging microRNA (miR)-1179. Taken together, the present study has revealed the existence of a novel TMPO-AS1/miR-1179/TRIM37 molecular axis conferring DOC resistance of breast cancer cells, thereby suggesting a promising novel therapeutic target for breast cancer.