Reduction of miR-132-3p contributes to gastric cancer proliferation mainly by targeting MUC13

Abnormal expression of EGFR signaling and miRNAs has been widely seen in gastric cancer. This study mainly focuses on the miRNAs that regulate HER activation through MUC13. The expression of MUC13 was explored using western blot assay or immunohistochemistry. Bioinformatic predictions were conducted using TargetScan. Luciferase reporter assay and western blot were performed to determine whether miRs target MUC13. MiR mimics or inhibitors were used to enhance or inhibit miRNA expression. The effect of miRs or MUC13 on cell proliferation, colony formation and migration were analyzed. The protein level of MUC13 was significantly increased in gastric cancer tissues compared with normal tissues. TargetScan predictions indicated that MiR-212-3p and miR-132-3p may bind to the 3'-untranslated region of MUC13. Further study revealed that miR-132-3p was significantly decreased in gastric cancer tissues, while miR-212-3p showed no obvious changes. Luciferase assay and western blot validated that MUC13 was a target gene of miR-132-3p. Inhibition of miR-132-3p enhanced gastric cancer cell proliferation, colony formation and migration through activation of HER2, ERK and Akt, which was similar with the effect of MUC13 overexpression. Inhibition of MUC13 could reverse miR-132-3p inhibition-induced effects. In summary, reduction of miR-132-3p contributes to gastric cancer proliferation mainly by targeting MUC13.