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. 2021 Mar 5;12(3):250. doi: 10.1038/s41419-021-03539-5

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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 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. 7 — A, B HN9-S cells were totally ablated of endogenous p62 using the CRISPR/Cas9 system (p62 KO), after which a reversal construct of wild type p62 was transiently transfected to p62 KO cells (p62 recons). Clonogenic survival (A) and percentage of cells positive for SA-β-gal staining (B) in HN9-S and p62 gene-edited HN9-S cells after irradiation (n = 3). Results are presented as means ± standard error of the mean (SEM). ***p < 0.005. C Overview of the different epigenetic regulation of p62 expression and the survival responses against irradiation in subclones, HN9-R and HN9-S, within a radio-resistant head and neck cancer tumor.