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. 2022 May 25;22:201. doi: 10.1186/s12935-022-02545-7

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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. 4 — PGM1 knockdown promoted cell proliferation and arrested more cells in S phase. A PGM1 overexpression markedly inhibited the proliferation of HT29 and SW620 cells, while knockdown of PGM1 markedly promoted the proliferation of HT29 and SW620 cells. B Colony formation abilities of the CTRL, OE-NC, OE-PGM1, shCTRL, and shPGM1 groups of HT-29 and SW620 cells; C EdU assays comparing the proliferation of CTRL, OE-NC, OE-PGM1, shCTRL, and shPGM1 groups of HT-29 and SW620 cells (scale bar = 100 μm). D Flow chart showing the cell cycle distribution of HT-29 and SW620 cells in the five different groups. Data are presented as a mean value ± SD of results obtained from three replicate samples; *P < 0.05, **P < 0.01, ***P < 0.001; ^##P < 0.01, ^###P < 0.001, ^####P < 0.0001