The Research Of Function And Mechanism Of LncRNA HOTAIR In Esophageal Squamous Cell Carcinoma

The dysregulation of long noncoding RNAs(lncRNAs) HOTAIR has been frequently reported in cancer studies and lead to the development and progression of tumor. However, the mechanism and its function in esophageal squamous cell carcinoma(ESCC)remains unclear. Many studies have confirmed the overavtivity of glycolysis is a significant biochemical characteristics of the tumor cells. Quantitative real-time PCR was carried out to detect the relative expression of HOTAIR in esophageal squamous cell carcinoma cell lines and tissues. KYSE30 cells were treated with si-HOTAIR or si-HK2 to investigate the role of HOTAIR in cell proliferation and metastasis. Higher expression of HOTAIR in ESCC tissues was associated with higher clinical stage,and was also correlated with shorter overall survival of patients with ESCC. Exogenous downregulation of HOTAIR expression significantly suppressed the in vitro cell-cycle progression, proliferation, and colony formation of gastric cancer cells and the development of tumors in nude mice.We found HOTAIR possibly inhibited miR-143,and miR-143 inhibited HK2 expression by targeting the 3’UTR of HK2 mRNA after bioinformatic prediction and Luciferase assay. The expression of miR-143 was upregulated over 2.9 fold after inhibition of HOTAIR. In addition, western blot results show that over expression mi R-143 or inhibition of HOTAIR can repress the expression of HK2 protein. Further more, a reverse correlation between the expression of miR-143 and HK2 protein was noted in ESCC tisssues. Our study shows that HOTAIR could contribute to esophageal carcinogenesis,then accelerated the expression of miRNA143-targeted-gene HK2 and executed glycolysis to promote the proliferation and tumorigenesis of esophageal squamous cell carcinoma cells.The HOTAIR/miR-143/HK2 interaction might serve as important targets for ESCC diagnosis and therapy.