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. 2024 Apr 18;14:8983. doi: 10.1038/s41598-024-59724-x

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© The Author(s) 2024

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 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/.

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The function of BRD3 on the proliferation, migration, and apoptosis of COAD cells. Notes: The results of qRT-PCR showed that si-BRD3-2 successfully knocked down the expression of BRD3 in HCT116 (A) and HT29 (B) cells. The knockdown of BRD3 inhibited the proliferation ability in both HCT116 (C) and HT29 (D) cells compared with the si-NC group. The depletion of BRD3 significantly repressed the migration of HCT116 (E, G) and HT29 (F, H) cells. (I) Flow cytometry showed that BRD3 knockdown could promote the apoptosis in HCT116 and HT29 cells. *p < 0.05, **p < 0.01, ***p < 0.001, p-value based on t-test. All experiments were implemented separately in triplicate.