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. 2020 Jan 15;10:357. doi: 10.1038/s41598-019-57047-w

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© The Author(s) 2020

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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Pro-tumoral action and molecular mechanism of SOX9 in cancer. In the context of non-tumor cells (left panel), SOX9 is able to promote neoplastic transformation through the induction of cell proliferation and the evasion of senescence. At the molecular level, this transformation takes place through the induction of BMI1 expression, which represses the expression of the tumor suppressors p16^INK4A and ARF (previously described by Matheu et al., 2012). In the context of tumor cells (right panel), generally deficient in p16^INK4A and ARF expression, SOX9 enhances tumor progression through the promotion of cell proliferation and the evasion of apoptosis and senescence. In this context, the molecular mechanism involves the repression of the tumor suppressor p21^CIP.