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. 2019 Feb 26;8(3):19. doi: 10.1038/s41389-019-0123-5

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© The Author(s) 2019

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 Cell cycle distribution was determined by flow cytometric analysis in HCT116 (left panel) and HT-29 cells (right panel) after CDCA5 knockdown. The percentage of cells in the G0/G1, S, and G2/M phases was calculated. ^*P < 0.05 vs. sh-Ctrl. b Western-blot analysis of CDK1 and CyclinB1 in HCT116 cells after transduction with sh-CDCA5 or sh-Ctrl lentivirus. The integrated band density was determined by ImageLab Software, and GAPDH as the internal control (^*P < 0.05). All experiments were performed in triplicate