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. 2017 Aug 7;7:7433. doi: 10.1038/s41598-017-07964-5

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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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JAM-A activated TGF-β/NODAL signaling. (A,B) In JAM-A-transfected DB cells (A) and DLBCL patients (B), JAM-A overexpression was related to activation of TGF-β/NODAL signaling. (C) As assessed by Whole-mount in Situ Hybridization and real-time quantitative RT-PCR, ndr-1 and ndr-2 were increased in jam-1-overexpressing zebrafish. WT, wild type. (D) JAM-A upregulated NODAL expression, which was restored by specific TGF-β/NODAL/Smad inhibitor SB431542 or JAM-A ShRNA. SB431542 abrogated JAM-A-induced lymphoma cell invasion (E) JAM-A was the highest in patients with involvement of endoderm-derived organs, followed by those with involvement of mesoderm- and ectoderm-derived organs. (F) JAM-A correlated with increased NODAL expression in primary lymph nodes, as well as in secondary lesions. Data in (C) are representative of three independent experiments.