lncRNA HOTAIR upregulates COX-2 expression to promote invasion and migration of nasopharyngeal carcinoma by interacting with miR-101

Background: Nasopharyngeal carcinoma (NPC) is the most common type of head and neck cancers which is notable for its distinctive pattern of geographical distribution. HOTAlR has been reported to regulate nasopharyngeal carcinoma tumorigenesis and progression. However, the detailed mechanism underlying HOTAlR-promoted nasopharyngeal carcinoma remains not fully understood. Methods: We used RT-qPCR approach to examine genes expression and mRNA level. MTT assay and soft agar assay were used to detect cell growth rate in culture and under suspended condition, respectively. Besides, we employed wound healing assay and transwell invasion assay to determine migration and invasion ability of nasopharyngeal carcinoma cells. We predicted direct downstream targets of miR-101 by bioinformatic analysis, which was confirmed by dual luciferase reporter assay. Results: HOTAlR was upregulated in NPC tissues and cells. miR-101 inhibitor greatly enhanced HOTAIR knockdown-regulated cell proliferation, migration and invasion of CNE1 and CNE2 cells. miR-101 was shown to directly bind 3'UTR of COX-2 and downregulate COX-2 expression. Finally, COX-2 overexpression was demonstrated to rescue the tumor phenotypes of nasopharyngeal carcinoma cells attenuated by HOTAlR knockdown or miR-101 mimic. Conclusions: Here, we highlight the importance of HOTAlR/miR-101 /COX-2 axis in progression of naso-pharyngeal carcinoma cells. Our findings provide a novel mechanism for explaining HOTAlR-induced nasopharyngeal carcinoma and help developing the therapeutical strategies by targeting HOTAlR. (C)2018 Elsevier Inc. All rights reserved.