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. 2020 Sep 8;11:4455. doi: 10.1038/s41467-020-18259-1

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© The Author(s) 2020

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a Western blot verification of the knockdown (KD) or overexpression (OE) of MTA1 in the HCT116 cells. Shown is representative of three independent repeats with similar results. b, c Flow cytometry measurement of the mitotic-arrest cell proportion in MTA1-deletion, control or MTA1-overexpression HCT116 cells after nocodazole treatment for 6 h and 12 h. Propidium Iodide (PI) was used to stain the nuclear DNA, and the G2/M cells were marked with 4 N DNA content. d, e Flow cytometry measurement of the mitotic-arrest cell proportion after the nocodazole treatment for 6 h, 12 h and 18 h. The mitotic cells were marked by antibody against mitosis-specific phosphorylated Histone 3. f Flow cytometry measurement of the mitotic-arrest cell proportion in control and EGFP-MTA1 stably expressing HCT116 cells after nocodazole treatment for 18 h. g The overexpression of MTA1 in the KYSE-410 cancer cells also resulted in a lower mitotic arrest by nocodazole. c, e Data are represented as mean ± SD, n = 3 per group.