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. 2023 Mar 4;14:1244. doi: 10.1038/s41467-023-36755-y

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© The Author(s) 2023

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a Schematic representation of the p53 protein structural domains and localization of four distinct p53 DNA-contact mutations (R248W, E258K, P278F and E286K). b D2 mRNA expression was measured by Real-Time PCR in SCC011 cells transiently transfected with four DNA-contact mutant p53 plasmids, carrying different p53 DNA-mutations (R248W, E258K, P278F and E286K) (n = 3 independent experiments). c, d Transient co-transfection of a Dio2-LUC-WT promoter (c) and TRE3-TK-LUC (d), with four distinct mutant p53 plasmids, in SCC011 cells (n = 3 independent experiments). e Characteristics of two human SCC cancer cell lines with different endogenous p53 status, SCC011 (p53 wild-type status) and SCC13 (p53 mutant status). f, g D2 mRNA expression was measured by Real-Time PCR in SCC011 (f) and SCC13 (g) cells, in a time course response to DNA damage induced by exposure to UV-C radiation (100 µJ/cm²) at the indicated time points (0, 1, 2, 4 and 8 h) (n = 3 independent experiments). h Western Blot analysis of cell cycle (Cyclin-D1), apoptosis (BCL-2, BAX) and regulatory proteins (ATM, phospho-ATM Ser-1981, p53, phospho-p53 Ser-15, p21) in SCC011 cells following exposure to UV-C radiation. Cell lysates were analyzed at the indicated time points (0, 1, 2, 4, and 8 h) after treatment. A representative result of 3 independent experiments is shown. GAPDH and PCNA were used as internal markers. i, j D2 mRNA expression was measured by Real-Time PCR in SCC011 (i) and SCC13 (j) cells, in a time course response to DNA damage induced by exposure to UV-A/B radiation (30 mJ/cm²) at the indicated time points (0, 4 and 8 h) (n = 3 independent experiments). k, l Western Blot analysis of regulatory proteins (ATM, phospho-ATM Ser-1981, p53, phospho-p53 Ser-15) in SCC011 (k) and SCC13 (l) cells following exposure to UV-A/B radiation. Cell lysates were analyzed at the indicated time points (0, 4, and 8 h) after treatment. A representative result of 3 independent experiments is shown. m Schematic representation of mechanism of action of two antitumor drugs, KuDOS (KU-55933) and etoposide, and their effects on the activation of ATM serine/threonine kinase and p53 protein. n, o D2 mRNA expression was measured by Real-Time PCR in SCC011 (n) and SCC13 (o) cells, treated with etoposide (50.0 µM/30 min) and KuDOS (100.0 µM/1 h) as single drugs or used in combination (n = 3 independent experiments). All the results are shown as means ± SD from at least 3 separate experiments. p-values were determined by two-tailed Student’s t-test. *p < 0.05, **p < 0.01, ***p < 0.001. Source data are provided as a Source data file.