LncRNA XIST Promotes Proliferation, Migration and Invasion of Esophageal Squamous Cell Carcinoma Cells via Regulation of miR-186-5p/ZEB1

Background/Aim: Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) are crucial molecules for tumor progression in various human cancers. However, the function of lncRNA X-inactive specific transcript (XIST) in esophageal squamous cell carcinoma (ESCC) remains to be determined. The current study aimed to explore the function and molecular mechanism of lncRNA XIST in ESCC progression. Materials and Methods: The expression level of lncRNA XIST in ESCC cell lines was measured by qRT-PCR. The effects of lncRNA XIST on cell proliferation, migration, and invasion on ESCC were detected by CCK-8, transwell, and scratch assays. The expression levels of proteins were determined by western blot and luciferase reporter assays were used to identify specific target relationships. Results: LncRNA XIST was overexpressed in ESCC cell lines when compared to normal cell lines. The inhibitor of lncRNA XIST markedly inhibited ESCC cell proliferation, migration, and invasion. Furthermore, miR-186-5p was down-regulated in ESCC cells. LncRNA XIST could sponge miR-186-5p and knockdown of lncRNA XIST could increase the expression of miR-186-5p. We also confirmed Zinc finger E-box binding homeobox 1 (ZEB1) as the target for miR-186-5p, while overexpression of ZEB1 reversed the effects of miR-186-5p inhibition on the malignant behavior of EC9706 and KYSE30 cells. Conclusion: Our data revealed that lncRNA XIST promotes ESCC metastasis by regulating the miR-186-5p/ZEB1 axis. This study may provide a theoretical basis for the molecular mechanisms involved in esophageal cancer.