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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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Lenalidomide inhibited lymphoma progression. (A) Lenalidomide (1 μM) downregulated JAM-A and NODAL expression more significantly in JAM-A-transfected DB cells as compared to vector-transfected cells. (B,C) Lenalidomide (1 μM) inhibited JAM-A-transfected cell invasion (B) and EMT (C). (D) In murine xenograft model established with subcutaneous injection of DB cells, tumor size was similar between vector-transfected (Vector) and JAM-A-transfected (JAM-A) group. Lenalidomide (25 mg/kg/day, JAM-A + lenalidomide) retarded tumor growth. *P < 0.05 and ***P < 0.001 comparing with the JAM-A group. (E) By micro-PET-CT, JAM-A overexpression contributed to tumor metastasis, all involving endoderm- and mesoderm-associated organs, which was inhibited by lenalidomide. (F) Lenalidomide downregulated JAM-A and NODAL expression. Data in (B) and (C) are representative of three independent experiments.