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. 2020 Dec 28;12(1):162–171. doi: 10.1080/21655979.2020.1863014

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© 2020 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 License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — MRPL23-AS1 serves as a sponge of miR-30b in OS cells. (a) RNA pull-down assay using biotin-labeled MRPL23-AS1 probe, followed by qRT-PCR analysis of enrichment of miR-30b, miR-596 and miR-760. (b) The wild-type or mutant binding site between MRPL23-AS1 and miR-30b. (c) Luciferase reporter gene assay detecting the luciferase activity of wild-type or mutant MRPL23-AS1 vector after miR-30b overexpression. (d) qRT-PCR analysis of miR-30b expression after overexpression or silencing of MRPL23-AS1. (e) qRT-PCR analysis of miR-30b expression in control or MRPL23-AS1-silenced xenograft tumor tissues. (f) qRT-PCR analysis of miR-30b expression in OS and matched normal tissues. (g) The correlation between MRPL23-AS1 and miR-30b in OS tissues. (h) FISH assay showing the co-location between MRPL23-AS1 and miR-30b in OS cells. **p < 0.01, ***p < 0.001