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. 2022 Mar 28;12:38. doi: 10.1186/s13578-022-00772-z

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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. 2 — MIR210HG promotes proliferation of breast cancer. A Proliferation ability of MCF-7 and MDA-MB-231 cells were measured by MTT assay after transfected MIR210HG siRNA. The results were normalized to scrambled siRNA group. B Proliferation ability of MCF-7 and MDA-MB-231 cells were measured by MTT assay after MIR210HG was induced by DOX. The results were normalized to 0 h time point. C and D Colony formation assay analysis of MCF-7 and MDA-MB-231 cells after silencing and overexpression MIR210HG respectively. E Expression of Ki-67 was determined by immunohistochemistry (IHC) of 6 specimens of breast cancer patients. Scar bars: 100 μm. F Xenograft tumors of 4 groups: scrambled siRNA MDA-MB-231 cell; MIR210HG siRNA MDA-MB-231 cell; 231^{MIR210HG−OV} cell without DOX treatment; 231^{MIR210HG−OV} cell with DOX treatment. **p < 0.01, ***p < 0.001