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. 2021 Feb 24;11:4480. doi: 10.1038/s41598-021-83979-3

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© The Author(s) 2021

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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Overexpression of TKT induces resistance to APR-246 in p53-null cells and protects against APR-246-induced superoxides. (A) TKT mRNA expression and (B) western blots for TKT in H1299 parental (p53^null), p53^R273H and p53^R175H cells with either TKT or red fluorescent protein (RFP) overexpression. (A) Expression normalised to RFP, (B) actin is shown as loading control. (C) Cell viability and (D) proliferation of H1299 parental (p53^null) cells with either TKT or red fluorescent protein (RFP) overexpression following 72 h APR-246 treatment (15 µM). (E) Geometric mean fluorescence intensity of MitoSOX Red in H1299 parental (p53^null) cells either untransfected (Parental) or overexpressing TKT (TKT cDNA) with 18 h APR-246 treatment (25 µM) measured with flow cytometry. Data represent mean, error bars = SEM, n = 3 for all studies excluding (B) where blots are representative of 2 independent experiments. (A) Unpaired Student’s t-test on raw data. (C,E) One-way ANOVA with Dunnett’s multiple comparison post-test. (D) Unpaired Student’s t-test. ns, not significant; *p < 0.05, ***p < 0.001, ****p < 0.0001.