Kun Zhuang1,2, Qiang Wu2, Chun-Shun Jin1, Hui-Jun Yuan2, Jin-Zhang Cheng1. 1. Department of Otolaryngology, Head and Neck Surgery, the Second Hospital of Jilin University, Changchun, Jilin, China. 2. Department of Otolaryngology, Head and Neck Surgery, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
Abstract
BACKGROUND: 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. OBJECTIVE: In this study, we examined the role of HNF1A-AS in NPC progression in vitro and in vivo. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: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. OBJECTIVE: In this study, we examined the role of HNF1A-AS in NPC progression in vitro and in vivo. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
Entities:
Keywords:
HNF1A-AS; Long non-coding RNA; RNAi; metastasis; nasopharyngeal carcinoma; proliferation