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. 2023 May 27;18(1):2217033. doi: 10.1080/15592294.2023.2217033

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© 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Figure 6. — Schematic of molecular mechanism.Note: METTL3 promoted the expression of lncKCNQ1OT1 by regulating its m6A modification. While the up-regulated lncKCNQ1OT1 played the role of ceRNA in the targeted inhibition of miR-103a-3p, and MDR1, as the downstream molecule targeting miR-103a-3p, could enhance DOX resistance of breast cancer.