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. 2021 Mar 10;40:92. doi: 10.1186/s13046-021-01889-8

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© The Author(s) 2021

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. 8 — MT-RNR1 overexpression reversed inhibited cell proliferation and increased cell apoptosis caused by ZNF582-AS1 overexpression. a and b EdU assay and c CCK-8 assay determined cell proliferation of MT-RNR1-overexpressed-ZNF582-AS1-overexpressed OSRC2 and Caki-1 cells comparing with their control cells. d and e TUNEL assay and f and g flow cytometry determined cell apoptosis of MT-RNR1-overexpressed-ZNF582-AS1-overexpressed OSRC2 and Caki-1 cells comparing with their control cells. h Tumors collected from mice are shown. i and j Tumor volume curves and tumor weights of the MT-RNR1-overexpressed-ZNF582-AS1-overexpressed and control groups were measured and compared. k and l The cell proliferation and apoptosis of tumor were examined