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. 2022 Jan 10;17:4. doi: 10.1186/s13062-021-00314-6

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — LINC00885/miR-3150b-3p/BAZ2A axis regulated cell proliferation and apoptosis in CC. A BAZ2A was silenced by transfection of sh-BZA2A#1/2/3 in HeLa cells as indicated in RT-qPCR and western blot analyses. HeLa cells were transfected with sh-Ctrl, sh-LINC00885#1, sh-LINC00885#1 + miR-3150b-3p inhibitor, or sh-LINC00885#1 + miR-3150b-3p inhibitor + sh-BAZ2A#1 respectively for subsequent assays. B–D CCK-8, EdU and colony formation assays were done to detect proliferation of HeLa cells transfected with indicated plasmids. E–F TUNEL assay and western blot analysis of expression levels of apoptosis-related genes (cleaved and total caspase 3 and caspase 9) were done to determine apoptosis of HeLa cells under different transfection conditions. *P < 0.05, **P < 0.01