ERK3 is transcriptionally upregulated by ?Np63? and mediates the role of ?Np63? in suppressing cell migration in non-melanoma skin cancers

Abstract Background p63, a member of the p53 gene family, is an important regulator for epithelial tissue growth and development. ?Np63? main isoform p63 highly expressed in Non-melanoma skin cancer (NMSC). Extracellular signal-regulated kinase 3 (ERK3) atypical mitogen-activated protein (MAPK) whose biochemical features cellular regulation are distinct from those conventional MAPKs such as ERK1/2. While ERK3 has been shown to be upregulated lung cancers head neck cancers, which it promotes cell migration invasion, little known about implication NMSCs. Methods Fluorescent immunohistochemistry was performed evaluate expression levels ?Np63? normal NMSC specimens. Dunnett’s test compare mean fluorescence intensity (MFI, indicator levels) or between cutaneous samples samples. A mixed effects (ANOVA) used determine correlation (MFI). The by studied qRT-PCR, Western blot luciferase assay. effect on measured performing trans-well Results level NMSCs compared tissue. significantly AK SCC comparison there strong positive specimens patients with AK, BCC. Further, we found that positively regulates transcript A431 HaCaT cells, underlying upregulation its Moreover, similar depletion, silencing greatly enhanced migration. Restoration under condition counteracted increase induced depletion ?Np63?. Mechanistically, inhibits phosphorylation Rac1 G-protein formation filopodia cells. Conclusions regulated mediates role suppressing NMSC.