本研究旨在探讨长链非编码RNA LINC01559对乳腺癌（BCa）多西他赛抗药性的调控作用及其潜在机制。本研究发现LINC01559表达上调，LINC01559过表达促进了BCa细胞对多西他赛的抗药性。此外，研究揭示了LINC01559在BCa细胞中的上调是由FTO介导的m6A-YTHDF2依赖性去甲基化引起的。另外，双荧光素酶报告基因实验证实了LINC01559与miR-1343-3p的结合能力，并且Pearson相关分析显示二者之间存在负相关。尤其值得注意的是，miR-1343-3p的抑制在一定程度上消除了LINC01559沉默引起的BCa细胞对多西他赛抗药性的抑制。总之，FTO介导的表观遗传上调LINC01559通过负调控miR-1343-3p促进BCa细胞对多西他赛的抗药性。 © 2023 The Authors. The Kaohsiung Journal of Medical Sciences由John Wiley & Sons Australia有限公司代表高雄医科大学出版。

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.© 2023 The Authors. The Kaohsiung Journal of Medical Sciences published by John Wiley & Sons Australia, Ltd on behalf of Kaohsiung Medical University.