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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 2. — Lnc KCNQ1OT1 depletion restrained DOX resistance in BC cells and DOX-resistant BC cells via elevating miR-103a-3p.Note: sh-lnc KCNQ1OT1 was transfected into DOX-resistant BC cells. a, qRT-PCR was employed to detect transfection efficiency and miR-103a-3p expression. b, cell viability was determined by MTT. c, the capability of cell proliferation was detected using clone formation. d, the apoptosis rate was measured with flow cytometry. e, western blot was performed to measure Bax, Bcl-2 expression. f, the mutual binding site between lnc KCNQ1OT1 and miR-103a-3p was predicted by starbase, and the interplay between lnc KCNQ1OT1 and miR-103a-3p was validated by dual-luciferase reporter gene assay and RIP assay.