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. 2022 Jun 9;21:125. doi: 10.1186/s12943-022-01603-y

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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 — CBX2 silencing alters leukemic cell survival and induces cell death. A and B Proliferation assay with shCBX2#1, shCBX2#2, and shSCR in U937 (A) and K562 (B) cells; experiments were performed at 7 days of puromycin selection; error bars show SD of three biological replicates (*P < 0.05, **P ≤ 0.01). C and D CCK8 assay of CBX2 knock-down and shSCR-transduced U937 (C) and K562 (D) cells; experiments were performed at 7 days of puromycin selection; error bars show SD of three biological replicates (*P < 0.05, **P ≤ 0.01). E and F Percentage of PI-positive shCBX2- and shSCR-transduced U937 (E) and K562 (F) cells; experiments were performed at 7 days of puromycin selection; error bars show SD of three biological replicates (*P < 0.05, **P ≤ 0.01)