Abstract
This study aimed to explore the role of micorRNA-2053 in esophageal cancer development. The expression level of miR-2053 in esophageal cancer cell lines was detected. After cell transfection, the effects of miR-2053 overexpression on proliferation, apoptosis, migration and invasion of esophageal cancer cells were determined. Moreover, the potential molecular mechanism was explored by measuring the epithelial-mesenchymal transition (EMT) and apoptosis-related proteins. Luciferase reporter assay was conducted to investigate the target gene of miR-2053. The protein expressions of PI3K/AKT pathway associated factors were detected after overexpression of miR-2053 or administration with the pathway inhibitor LY294002. The miR-2053 was downregulated in esophageal cancer cell lines. Overexpression of miR-2053 inhibited cell proliferation, migration and invasion while promoted apoptosis. Molecular mechanism elucidated that miR-2053 could reduce EMT and elevate the expression of pro-apoptotic proteins. Further study found that overexpressed miR-2053 could negatively regulate KIF3C and involve in PI3K/AKT signaling pathway. Our study demonstrated the downregulation of miR-2053 in esophageal cancer. Downregulation of miR-2053 involved in the proliferation, apoptosis, migration and invasion of esophageal cancer cells through upregulating KIF3C expression and activating the PI3K/AKT signaling pathway. miR-2053 may have the potential in clinical treatment of esophageal cancer.