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. 2020 Feb 18;20:55. doi: 10.1186/s12935-020-1135-0

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© The Author(s) 2020

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 — CAV-2 overexpression partially restores BRD4-siRNA mediated cell proliferation. a Western blot was employed to detect BRD4, CAV-2, PCNA, C-myc, CDK2, and pRb expression when cotransfected CFPAC-1 and PANC-1 cells with BRD4 nc/siRNA and CAV-2 ctrl/over plasmid. BRD4 decreased PCNA, C-myc, CDK2, and pRb expression. CAV-2 overexpression can partially reverse the protein expression of BRD4 suppression. b, c. Sulforhodamine B assays (b) and plate clone formations (c) showed that CAV-2 overexpression partially reversed decreased cell proliferation of BRD4 knockdown. d Cell cycle experiments showed that suppression of BRD4 induced G1 phase arrest. CAV-2 overexpression can partially reverse the effects of BRD4 knockdown. The asterisk indicates that p is less than 0.05