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. 2022 Jun 11;41:198. doi: 10.1186/s13046-022-02412-3

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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. 5 — NCAPD3 promoted CRC cell proliferation, migration and tumor metastasis. A-C Cell viability, colony formation and migration were measured by CCK8 assay, colony formation assay and wound-healing assay after NCAPD3 overexpression or knockdown. Scale bar: 50 μm. D-F CCK-8 assay, colony formation analysis and wound-healing assay were performed under different transfections as indicated in figures. Scale bar: 50 μm. G Representative images of HE staining of lung tissues in NCAPD3-overexpressed and control group, n = 5. Scale bar: 50 μm. H Representative Ki67 IHC staining of lung tissues from mice, n = 5. Scale bar: 20 μm. NC3 represents NCAPD3, shCTRL represents shcontrol, shNC3 represents shNCAPD3, siNC represents negative control siRNA. All experiments were implemented three times. Student’s t-test was used to analyze the data (*P < 0.05, **P < 0.01, ***P < 0.001)