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. 2020 Mar 4;19:51. doi: 10.1186/s12943-020-01174-w

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© The Author(s) 2020

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. 3 — Silencing MIR22HG promotes colorectal cancer cell proliferation and metastasis in vitro. a, Representative images and bar graphs showing the effects of MIR22HG knockdown on colony formation in HCT116. b, Effects of MIR22HG knockdown on colorectal cancer cell proliferation were measured by CCK-8 assays. c, Representative images and bar graphs depicting the migration and invasion abilities of MIR22HG–silenced HCT116 cells. d-f, Effects of MIR22HG overexpression on colony formation (d), cell proliferation (e) and migration (f) in LoVo