MicroRNA-140-5p suppresses cell proliferation and invasion in esophageal squamous cell carcinoma by targeting Glut1

Abstract

Objective: To investigate the expression of microRNA-140-5p (miR-140-5p) in esophageal squamous cell carcinoma (ESCC) and its role in cell proliferation and invasion of ESCC. Methods: Real-time quantitative PCR (qPCR) was used to detect the expression levels of miR-140-5p in ESCC tissues and cells. Negative control and miR-140-5p mimic were transfected into Eca109 and KYSE70 cells. CCK-8 kit and Transwell assay were employed to examine the changes of cell proliferation and invasion ability after transfection, respectively. The dual-luciferase reporter assay was used to assess the interaction of miR-140-5p with Glut1. Western blot was utilized to detect the Glut1 protein expression after transfection. Results: Analysis of the related GEO datasets revealed that the expression of miR-140-5p in ESCC tissues was significantly lower than that in normal tissues (P<0.01). The qPCR testing demonstrated that the expression of miR-140-5p in ESCC tissues and cells was markedly lower than that in normal tissues and normal esophageal epithelial cell Het-1A (P<0.01). The miR-140-5p expression was closely associated with tumor differentiation, TNM staging and lymph node metastasis in ESCC patients. The survival rate of ESCC patients with high miR-140-5p level was higher than those with low miR-140-5p level (P<0.05). Besides, addition of miR-140-5p mimic significantly upregulated the expression of miR-140-5p in Eca109 and KYSE70 cells, and suppressed cell proliferation and invasion in Eca109 and KYSE70 cells. The dual-luciferase reporter assay showed that Glut1 was a direct target of miR-140-5p in ESCC cells, and its expression was upregulated in ESCC tissues. Glut1 expression was inversely associated with miR-140-5p expression in ESCC tissues. MiR-140-5p mimic dramatically inhibited the expression of Glut1 in Eca109 and KYSE70 cells. Conclusions: MiR-140-5p plays an essential role in ESCC development and progression. Targeting at miR-140-5p/Glut1 may be a novel therapeutic strategy for ESCC patients.