Fig. 5: The interaction of PAK2 and SOX2 regulates the downstream DEK gene.

A qRT-PCR to determine the expression of DEK in human LSCC cells and normal lung epithelial cells, *p < 0.05 versus BEAS-2B cells; B IHC assay to determine the expression of DEK in LSCC tissues and adjacent normal tissues; *p < 0.05 versus adjacent normal tissues; C Binding sites of SOX2 and DEK predicted by the JASPAR database (http://jaspar.genereg.net/); D ChIP assay to examine the binding of SOX2 to DEK and SOX1 promoter region, *p < 0.05 versus IgG antibody group; E qRT-PCR to determine the expression of DEK in cells, *p < 0.05 versus the oe-NC or oe-NC + sh-NC group; F qRT-PCR and Western blot to measure the silencing efficiency of sh-PAK2 and DEK expression upon sh-PAK2 treatment; *p < 0.05 versus the sh-NC group; G ChIP assay to examine the binding of SOX2 and DEK promoter region after PAK2 knockdown, *p < 0.05 versus the sh-NC or oe-NC group; H Co-expression analysis of SOX2 and DEK in LSCC samples in TCGA database; I Co-expression analysis of PAK2 and DEK in LSCC samples in TCGA database. Measurement data were summarized as mean ± standard deviation. One-way ANOVA with Tukey’s post hoc test was adopted for comparison among data of multiple groups (for A, E). Paired t-test was used for comparison between LSCC tissues and adjacent normal tissues (for B), while unpaired t-test was used for comparison between data of two groups (for D, F, G). Cell experiment was repeated three times.