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. 2021 Oct 20;11:746789. doi: 10.3389/fonc.2021.746789

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Copyright © 2021 Chen, Guo, Guo, Wu, Si, Xu, Kang and Sun

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The m6A–non-coding RNA model in drug-resistant cancer. (A) m6A–miRNA model: m6A modification directly affects the pre-miRNA splicing, resulting in abnormal miRNA level changes in cancer drug resistance. (B) m6A–lncRNA model: ARHGAP5-AS1 recruits METTL3 to promote the stability of ARHGAP5 for inhibiting drug-induced apoptosis. (C) In sorafenib-resistant liver cancer cell, m6A modification promoted circRNA-SORE stabilization. Then, circRNA-SORE could directly bind YBX1 protein or sponge miR-660-3p and miR-103a-2-5p for arresting drug-activated apoptosis.