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. 2018 Oct 23;38(10):1734–1750. doi: 10.1038/s41388-018-0546-z

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© The Author(s) 2018

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. 4 — Phospo-Lck is expressed in human glioblastomas and inhibition of phospho-Lck results in inhibition of paxillin and CrkII activation and loss of pseudopodia formation in hGCs. a Analysis of TCGA database shows that Lck mRNA is significantly upregulated in glioblastomas compared to Grade II and III tumors. In addition, the expression of Lck mRNA is significantly higher in glioblastomas with wild type IDH as compared to mutated IDH or tumors with mutated IDH and 1p/19q co-deletion (*p < 0.0001, One-way Anova). b Immunohistochemistry using pLck-Tyr394 antibody shows widespread expression of pLck in human glioblastoma tissue sections. c and d hGCs isolated from two patients with glioblastomas (hGC1 and hGC2) were left untreated or treated with 500 nM Lck-I for 2 h. Lysates were analyzed for phospho(Y394)-Lck, phospho(Y118)-paxillin, phospho(Y221)-CrkII, and the corresponding non-phosphorylated proteins as loading controls. Treatment with Lck-I significantly reduced the phosphorylation levels of Lck, paxillin, and CrkII (graph shows individual densitometric measurements from three experiments, the bars represent mean values ± s.d., *p < 0.05 with two-tailed Student’s t-test). e hGCs were stained for phalloidin-rhodamine and phospho(Y118)-paxillin (green) to identify pseudopodia and active paxillin. Paxillin phosphorylation was reduced in Lck inhibitor-treated cultures from the tips of hGC pseudopodia as compared to control cultures. Insets show individual control cells with positive p-Paxillin at the tips of pseudopodia while in Lck-I-treated cells we did not observe p-Paxillin or the formation of pseudopodia. f Numbers of pseudopodia per cell were counted (30 cells per well, individual measurements from 12 independent wells are plotted, bars represent mean values ± s.d.). Treatment with Lck inhibitor significantly reduced the number of pseudopodia per cell (p < 0.05, calculated with two-tailed Student’s t-test). Scale bars represent 200 μm