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. 2022 Jan 24;41:33. doi: 10.1186/s13046-021-02230-z

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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 — Knockdown of RPS27a regulates p53 activity without affecting its stability in response to stress. A NC and RPS27a knockdown of A549 cells were treated with 5 nM ActD for 6, 12 or 24 h; the protein expression was then detected with IB. B, C The NC and RPS27a knockdown A549 cells were treated with 5 nM ActD for a total of 24 h together with 50 μg/mL CHX for the indicated time periods; protein expression was then detected with IB. The expression of p53 in ActD and CHX-treated cells was quantified (p53/β-actin) and normalized to p53 at time 0 h; values were set at 1.0 for NC and RPS27a knockdown cells (n = 3) (C). D NC and RPS27a knockdown A549 cells were treated with 30 nM Dox for 6, 12 or 24 h, and the protein expression was detected with IB. E NC and RPS27a knockdown A549 cells were treated with 30 nM Dox for a total of 24 h together with 50 μg/mL CHX for the indicated time periods; the protein expression was then detected with IB. F The expression of p53 in Dox and CHX-treated cells was quantified (p53/β-actin) and normalized at time 0 h, with values set at 1.0 for NC and RPS27a knockdown cells (n = 3). G NC and RPS27a knockdown A549 cells were treated with 30 nM Dox for 24 h, and the expression of mRNA levels was analyzed with real-time PCR for the indicated time points (n = 3). H-J NC and RPS27a knockdown A549 cells were treated with 30 nM Dox for 24 h. The cell cycle percentage was analyzed with flow cytometry. ***p < 0.001 was calculated with ANOVA (n = 3) (H). Colony formation, observed and calculated (I). *p < 0.05, ***p < 0.001 was calculated with ANOVA (n = 3) (J). K-N NC and RPS27a knockdown A549 cells were seeded into the Transwell chamber and then treated with 30 nM Dox for 24 h. The invasion of cells in the lower chamber was observed, and the number of cells was counted (K). **p < 0.01, ***p < 0.001 were calculated with ANOVA (n = 3) (L). The migration of cells in the lower chamber was observed, and the number of cells was counted (M). ***p < 0.001 was calculated with ANOVA (n = 3) (N). NC, negative control; ActD, dactinomycin; Dox, doxorubicin; CHX, Cycloheximide; IB, immunoblotting