LncRNA HOTAIR regulates the expression of E-cadherin to affect nasopharyngeal carcinoma progression by recruiting histone methylase EZH2 to mediate H3K27 trimethylation

Abstract Background In recent years, there has been increasing evidence for the function of long non-coding RNA (lncRNA) in nasopharyngeal carcinoma (NPC).. We aim to delve into the position of lncRNA HOTAIR, together with EZH2, E-cadherin and H3K27me3 in NPC and explore the related mechanisms. Methods RT-qPCR and western blot analysis were carried out for detecting lncRNA HOTAIR, EZH2, E-cadherin and H3K27me3 expression in NPC tissues and cells. Moreover, the correlations between lncRNA HOTAIR and EZH2 expression and the clinicopathological characteristics and prognosis of patients with NPC were observed. NPC cell biological functions were examined through gain-of and loss-of function assays. RIP and ChIP assays were applied to detect whether lncRNA HOTAIR in NPC cells could regulate E-cadherin by recruiting EZH2 to mediate trimethylation of H3K27. Results LncRNA HOTAIR, EZH2, and H3K27me3 were richly expressed in NPC tissues and cells, and E-cadherin was lowly expressed. The prognosis of patients with overexpression of lncRNA HOTAIR and EZH2 was worse than that of patients with theirs low expression. Down-regulation of either HOTAIR or EZH2 inhibited cell proliferation, promoted apoptosis, suppressed migration and invasion and inhibited tumor growth. HOTAIR recruited histone methylase EZH2 to mediate trimethylation of H3K27 and regulated E-cadherin expression. Conclusion Our study suggests that lncRNA HOTAIR inhibits the expression of E-cadherin by stimulating the trimethylation of H3K27 by histone methylase EZH2 to promote cell migration, proliferation, and inhibit apoptosis of NPC cells.