Long non-coding RNA HNF1A-AS is upregulated and promotes cell proliferation and metastasis in nasopharyngeal carcinoma.

Abstract

Nasopharyngeal carcinoma (NPC) is a common head and neck cancer with an incidence of 10-30 cases per 100,000 in southern China. Although primary treatment includes radiation therapy, prognosis is still unsatisfactory. In this study, we examined the role of HNF1A-AS in NPC progression in vitro and in vivo. Relative levels of long non-coding RNA (LncRNA), HNF1A-AS, were evaluated in tumor tissues from 20 patients with NPC as well as from cultured NPC cell lines. Lentivirus-mediated HNF1A-AS knockdown was conducted in NPC cell lines, CNE-2 and SUNE-1. Cell migration and invasion abilities were estimated in vitro by colony-formation, wound-healing, and transwell assays. Cell cycle analysis was used to further examine the role of HNF1A-AS in cell proliferation. The tumor size of 24 male mice with or without HNF1A-AS knockdown was monitored once a week. The underlying mechanism of HNF1A-AS-mediated cell proliferation was studied by western blot analysis. Lentivirus-mediated HNF1A-AS knockdown suppressed cell proliferation and migration abilities. In mice injected with CNE-2 and SUNE-1, depletion of HNF1A-AS caused inhibition of tumor growth, whereas cell cycle analysis showed that HNF1A-AS-knockdown resulted in cell accumulation in the G0/G1 phase. Moreover, HNF1A-AS was found to be associated with epithelial to mesenchymal transition. Overall, our results suggest that LncRNA, HNF1A-AS potentially regulates NPC tumorigenesis. This could help in development of new strategies for NPC diagnosis and treatment.