Inhibition of miR-1303 suppresses the development of esophageal cancer by targeting CLDN18

Background Esophageal cancer is an aggressive malignant tumor, and its incidence rate is constantly increasing. Searching for a new biomarker is essential for the study of esophageal cancer. Methods The microRNA and messengerRNA expression levels were measured by employing RT-qPCR. The diagnostic value of miR-1303 in esophageal cancer was measured by the receiver operating characteristic curve. In TE-1 cells and KYSE520 cells, miR-1303 and CLDN18 were overexpressed or inhibited by transfection. The target of miR-1303 was forecasted by the TargetScan online database, which was identified by the dual-luciferase reporter system. The correlation between miR-1303 and CLDN18 in esophageal cancer was analyzed. Results MiR-1303 in esophageal cancer tissues increased and had a high diagnostic value in esophageal cancer. In TE-1 cells and KYSE520 cells, the overexpression of miR-1303 increased the proliferation and decreased the apoptosis, and the inhibition of miR-1303 decreased the proliferation and increased the apoptosis. The overexpression of miR-1303 significantly increased MMP2 and MMP9 and decreased E-cadherin in TE-1 cells and KYSE520 cells, and the inhibition of miR-1303 decreased MMP2 and MMP9 and elevated E-cadherin in TE-1 cells and KYSE520 cells. In esophageal cancer tissues, the expression of CLDN18 was significantly reduced, and CLDN18 was negatively correlated with miR-1303. In TE-1 cells and KYSE520 cells, the up-regulation of CLDN18 alleviated the progression of esophageal cancer caused by miR-1303. Conclusion MiR-1303 was increased in esophageal cancer tissue and had a high diagnostic value in esophageal cancer. MiR-1303 promoted the invasion and metastasis of esophageal cancer. In esophageal cancer, the inhibition of miR-1303 suppressed the development by targeting CLDN18.