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. 2023 Mar 15;14(3):197. doi: 10.1038/s41419-023-05722-2

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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. 6 — A Distribution of mutations in TSPYL2 gene according to sex in sex-related and somatic cancers. Statistical significance was calculated using Fisher’s exact test. B TSPYL2 expression in tumor vs matched normal pairs according to TNMplot tool. C Kaplan-Meier plots showing the percentage of patients who are alive at a time point in lung adenocarcinoma and osteosarcoma according to TSPYL2 expression level (high in red and low in blue). Statistical significance was calculated using log-rank test. D Graphical scheme of our proposed model. In unstressed conditions, TSPYL2 is maintained at low levels by MDM2-dependent proteasome degradation. In response to DNA damage TSPYL2 protein is stabilized and accumulates in non-transformed and in female cancer cells, but not in male cancer cells where SRY expression promotes the MDM2-dependent proteasome degradation of TSPYL2. The accumulated protein promotes the arrest of damaged cell growth.