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. 2017 Dec 1;7:16784. doi: 10.1038/s41598-017-17021-w

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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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Lck inhibition induces expression of S1PR1 on CLL cells and their migration toward S1P. (a) CLL cells from 10 cases were examined immediately, or were cultured for 16 h with either idelalisib (1 μM), Lck-i (1 μM) or left untreated. All cells were examined by flow cytometry for S1PR1 levels. (b) CLL cells from four patients were incubated for 16 h with idelalisib (1 μM), Lck-i (1 μM) or left untreated (None), and then examined for migration toward S1P using HUVEC-coated transwells. The data are presented as migration index which is the quotient of the number of CD19 + cells transmigrating in the presence of S1P divided by that in its absence. (c) CLL cells from four patients were cultured with ibrutinib (1 μM), Lck-i (1 μM) or left untreated (None), and examined for migration toward CCL21 using HUVEC-coated transwells. Data are presented normalised to the level of CCL21-induced migration observed with untreated cells which is taken to be 100%. Statistical significance for all parts of this figure was determined using a Student’s t-test for paired data.