Fig. 8.

Downregulated PLXNA1 modulated the ESCC cell biological properties via the involvement of the MAPK signalling pathway. ESCC cells were treated with DMSO, SB203580, LY3214996 and SP600125 in the presence of si-PLXNA1. (a) the proliferation of ESCC cells assessed by CCK-8 assay and analysed by repeated measures ANOVA; (b) the flow chart depicting cell cycle distribution in ESCC cells as assessed by flow cytometry; (c) the cell proportion/ratio in each cell-cycle phase; (d) the flow cytometry scatter plot of cell apoptosis in ESCC cells; (e) the ESCC cell apoptosis rate as determined by Annexin V/PI double staining; (f) the protein expression of Bcl-2 and BAX in the ESCC cells as determined by western blot analysis; (g) the grey value of Bcl-2 and BAX protein bands in the ESCC cells as determined by western blot analysis. ^⁎p < .05 vs. the si-PLXNA1 + DMSO group (cells treated with DMSO in the presence of si-PLXNA1). Measurement data were expressed as mean ± standard error of mean and analysed by one-way ANOVA, followed by Tukey's post hoc test; the experiment was repeated three times. ESCC, esophageal squamous cell carcinoma; miR-134, microRNA-134; ANOVA, analysis of variance; PLXNA1, plexin A1; NC, negative control.