FTO‐mediated epigenetic upregulation of LINC01559 confers cell resistance to docetaxel in breast carcinoma by suppressing miR‐1343‐3p

Abstract

Abstract This study was to explore the regulatory effect of long non‐coding RNA LINC01559 on Docetaxel resistance in breast carcinoma (BCa) and its underlying mechanism. In the present study, we found that LINC01559 expression was elevated and LINC01559 overexpression facilitated docetaxel resistance in BCa cells. Moreover, it was revealed that the upregulation of LINC01559 in BCa cells was induced by FTO‐mediated demethylation in an m6A‐YTHDF2‐dependent manner. Additionally, Dual‐luciferase reporter assay confirmed the binding ability between LINC01559 and miR‐1343‐3p, and Pearson correlation analysis showed a negative correlation between them. Particularly, miR‐1343‐3p inhibition partly abolished the suppression on docetaxel resistance in BCa cells caused by LINC01559 knockdown. To sum up, FTO‐mediated epigenetic upregulation of LINC01559 promoted cell resistance to Docetaxel in BCa by negatively regulating miR‐1343‐3p.

Keywords

• breast carcinoma
• docetaxel resistance
• FTO
• LINC01559
• N6‐methyladenosine