This study investigates the role of CPEB3 in esophageal cancer (EC) progression. The prognosis of EC patients was shown by survival analysis. CPEB3-targeting microRNAs were predicted by bioinformatics tools and further validated by dual-luciferase assay and RNA immunoprecipitation. CPEB3 expression in EC cell lines and EC tissues was analyzed by quantitative reverse transcription PCR. The viabilities of KYSE150 and EC9706 cells were measured by MTT and Cell Counting Kit-8 assays. The migration, invasion and tube formation of KYSE150 and EC9706 cells were examined by wound healing, Transwell and tube formation assay, respectively. E-cadherin, N-cadherin, fibronectin, vimentin and vascular endothelial growth factor (VEGF), epidermal growth factor receptor (EGFR) [and phosphorylation (p)] and STAT3 levels (and phosphorylation) in KYSE150 and EC9706 cells were determined by western blot analysis or quantitative reverse transcription PCR. In addition, a xenograft tumor model was established through subcutaneously implanting KYSE150 and EC9706 cells transfected with Lv-CPEB3 or Lv-control viruses. CPEB3 expression was downregulated in EC cells and tissues, and its overexpression inhibited viability, migration, invasion and the expressions of N-cadherin, fibronectin, vimentin and VEGF, EGFR, p-EGFR and p-STAT3 levels in KYSE150 cells, but promoted E-cadherin expression. Small interfering RNA (siRNA)-CPEB3 inversely affected these phenotypes and gene expressions in EC9706 cells. miR-106b-5p targeted CPEB3 and negatively regulated CPEB3 expression. miR-106b-5p mimics reversed the effect of CPEB3 overexpression on KYSE150 cells, and miR-106b-5p inhibitor reversed the effect of siRNA-CPEB3 on EC9706 cells. In mice, tumor volumes, weights and Ki-67 expression were lower in mice treated with Lv-CPEB3 than that with Lv-control. CPEB3 overexpressed by miR-106b-5p inhibition suppressed EC progression involved in EGFR and STAT3 signaling.
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