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. 2017 Jul 6;7:4770. doi: 10.1038/s41598-017-05047-z

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© The Author(s) 2017

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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A working model of the signaling mechanisms regulated by RA to induce NSCLC regression. RA treatment increases GATA6 expression levels in differentiated NSCLC cells. GATA6 acts (1) by inhibiting EGFR and CTNNB1 transcript, and (2) by activating the expression of the Wnt inhibitor FZD2. These molecular effects lead to the down-regulation of EGFR and Wnt signaling pathways, by arresting tumor cell proliferation and promoting cell differentiation.