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. 2015 May 7;8(10):16202–16219. doi: 10.18632/oncotarget.3892

Figure 2. p63 transcription factors modulate Src-focal adhesion kinase (FAK) signalling.

Figure 2

A. Microarray data of total p63, Src and PTK2/FAK mRNA levels in normal tissue and HPV-negative (p16-) and HPV-positive (p16+) oro-pharyngeal tumours. B. Correlation analysis of Src and PTK2/FAK against p63 in samples from (A). C. Relative mRNA levels of Src, PTK2/FAK and paxillin in human foreskin keratinocytes (HFK) expressing pBabe (control), early and late passage HFK expressing E6/E7 genes. D. Protein levels of total Src, FAK, paxillin, pSrc-Y416, pFAK-Y397, pFAK-Y576/577 and pPaxillin-Y118; E. cellular localisation (arrows) of total paxillin and pFAK-Y397 in aforementioned cells. F. Relative mRNA levels of PTK2/FAK and Src in p63 depleted cells and G. protein levels of total p63, Src, FAK, paxillin and pPaxillin-Y118 after transient knockdown by Scram (control) and two different p63 siRNA molecules in late passage E6/E7-HFK. β-actin served as loading control. Scale bars represent 50 μm. N = 3 independent experiments, mean ± SEM, ***p < 0.0001 compared to normal, ##p < 0.01 compared to the control, *p < 0.01 compared to the control, ††p < 0.01 compared to early passage E6/E7 HFK, ns: not significant.