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Fig. 6 | Molecular Cancer

Fig. 6

From: Identification of lymphocyte cell-specific protein-tyrosine kinase (LCK) as a driver for invasion and migration of oral cancer by tumor heterogeneity exploitation

Fig. 6

LCK inhibition promotes adherens junction formation. A SAS cells were transfected with non-targeting (siCtrl) or LCK-directed siRNAs (siLCK1, siLCK2) for 48 h or treated with DMSO, LCKi or dasatinib for 24 h. Confocal images show E-cadherin and F-actin localization in treated compared to non-treated cells. Maximum intensity projections of at least 6 optical sections are depicted (n = 3; scale bars = 10 μm). B Violin plots depict the enrichment factor of E-cadherin (left panel) and F-actin (right panel) at lateral contacts in SAS cells after knockdown or inhibition of LCK. About 500 individual bicellular contacts were measured. To determine statistical significances, one-way ANOVA was performed. C Western blot of protein lysates after 48 h of LCK knockdown or 24 h of LCK inhibitor treatment to analyze E-cadherin protein abundance. Rpl7 was used for loading control. (*p < 0.05, **p < 0.01, ***p < 0.001)

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Molecular Cancer

ISSN: 1476-4598