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Fig. 5 | Molecular Cancer

Fig. 5

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. 5

Inhibition of LCK leads to an upregulation of differentiation-associated genes. A Comparison of genes differentially expressed in OSCC metastasis versus primary tumors (m), high invasive SAS subclones versus weak invasive ones (c), Knockdown of LCK (s), LCKi (l) and dasatinib (d) treatment of SAS parental; genes at least significantly deregulated in three analyses are shown, significance of FDR < 0.05 are marked with a black square. Another filter criterion was the LCK correlation score (*), which includes the regulation direction considering the LCK expression levels or inactivation of LCK. B Venn diagram of genes significantly upregulated in metastasis or invasive clones and significantly downregulated upon LCK knockdown or inhibition via LCKi and dasatinib. C Venn diagram of genes significantly downregulated in metastasis or invasive clones and significantly upregulated upon LCK knockdown or inhibition via LCKi and dasatinib. D List of biological processes (Gene Ontology) that are significantly overrepresented in at least two LCK downstream analyses and more than 3-fold enriched. Skin differentiation-associated biological processes are marked in brown, neuron associated in green. E Significantly deregulated (at least in one analysis) genes of the superpathway “keratinization” (pathcards.com) are shown. To calculate the mean of LOG2(FC) across all analyses, the metastasis (m) and invasive SAS subclones analysis (c) were negatively taken into account. Significance is marked with a black square. F Confirmation of RNA-Sequencing data via RT-qPCR analysis for selected genes. PPIA and RPLP0 served a reference genes and normalization refers to siCtrl and DMSO (n = 3; one-way ANOVA; *p < 0.05, **p < 0.01, ***p < 0.001)

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