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. 2022 Sep 28;21:187. doi: 10.1186/s12943-022-01637-2

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© The Author(s) 2022

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/. 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. 3 — Knockdown of PCAF suppressed cell apoptosis and promoted proliferation in Hep3B cells. (A) The mRNA and protein expression of PCAF is down-regulated by siRNA structure against PCAF in Hep3B cells; (B) DAPI staining assay showed that knockdown of PCAF repressed cell apoptosis of Hep3B cells significantly (P = 0.002); (C) The activity of caspase 3/7 was decreased greatly by knockdown of PCAF in Hep3B cells (P = 0.002); (D) The percents of both early apoptotic cells and late apoptotic cells of Hep3B PCAF siRNA cells was decreased by around 50% as assessed by flow cytometry (P = 0.008); (E) Silencing PCAF was found to promote proliferation of Hep3B cells in BrdU incorporation ELISA assay apparently; (F) MTT assay displayed that knockdown of PCAF facilitated cell growth of Hep3B cells significantly