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. 2022 Feb 19;41(14):2095–2105. doi: 10.1038/s41388-022-02223-y

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© Crown 2022, corrected publication 2022

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. 8 — We show in this study that depletion of TSPAN6 cooperates with oncogenic RAS in tumorigenesis and that the tumor suppressor role of TSPAN6 requires P53. We show that TSPAN6 binds to and inhibits EGFR activation and thereby inhibits RAS activation. TSPAN6 does not bind to SCRIB or DLG1, suggesting that they act in parallel to each other in the regulation of the EGFR-RAS-ERK pathway, with TSPAN6 regulating EGFR and SCRIB/DLG1 regulating ERK. TSPAN6 also inhibits P38 activation by an unknown mechanism. TSPAN6 may be required for the activation of the tumor suppressor P53 by a pathway involving the activation of PI3K-AKT-TOR. Additionally, TSPAN6 alters epithelial cell morphology with its depletion leading to an EMT, which may further activate RAS-ERK signaling through SCRIB/DLG1 impairment. “?”, indicate that the potential involvement of TSPAN6 in these pathways needs to be confirmed.