Activation of PAR4 Upregulates p16 through Inhibition of DNMT1 and HDAC2 Expression via MAPK Signals in Esophageal Squamous Cell Carcinoma Cells
Effect of MAPK on DNMT1, HDAC2, and p16 expression by PAR4-AP in human ESCC cells. (a) Western blotting showing p16 protein levels in ESCC cell lines (EC109 and TE-1) with PAR4-AP treatment at 0, 1, and 2 h, respectively. (b) RT-PCR analysis showing p16 gene levels in ESCC cell lines (EC109 and TE-1) with PAR4-AP treatment at 0, 1, and 2 h, respectively. The results were calculated by normalizing to β-actin in the same sample with the ΔCt method. The changes in the relative mRNA levels are expressed as fold changes compared with the controls. (c) Western blotting showing p-ERK1/2 and p-p38 expression in ESCC cells with PAR4-AP treatment at 0, 1, 2, 6, 12, and 24 h, respectively. (d) Western blotting analyses for DNMT1, HDAC2, and p16 protein expressions in ESCC cells following treatment with PAR4-AP for 2 h and pretreatment with U-46619 (an activator of ERK1/2 and p38), tBHQ (an activator of ERK1/2), PD98059 (an inhibitor of ERK1/2), or SB203580 (an inhibitor of p38) for 60 min. The mean optic densities of the proteins were calculated by normalizing to GAPDH. All values are expressed as the means ± SEMs (). versus controls; versus PAR4-AP-only groups.
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