Abstract
Long noncoding RNA SLC9A3 antisense RNA 1 (SLC9A3‑AS1) plays a central role in lung cancer; yet, its functions in nasopharyngeal carcinoma (NPC) have not been elucidated. The present study revealed the roles of SLC9A3‑AS1 in NPC and dissected the mechanisms downstream of SLC9A3‑AS1. SLC9A3‑AS1 levels in NPC were assessed by applying RT‑qPCR. The modulatory role of SLC9A3‑AS1 interference on NPC cells was examined using numerous functional experiments. High expression of SLC9A3‑AS1 was observed in NPC samples. Patients with NPC with a high level of SLC9A3‑AS1 experienced a shorter overall survival than those with a low SLC9A3‑AS1 level. Loss of SLC9A3‑AS1 reduced NPC cell proliferation, colony formation, migration, and invasion but induced cell apoptosis in vitro. Animal experiments further revealed that the depletion of SLC9A3‑AS1 hindered NPC tumour growth in vivo. As a competitive endogenous RNA, SLC9A3‑AS1 sponged microRNA‑486‑5p (miR‑486‑5p), consequently upregulating E2F transcription factor 6 (E2F6). Finally, the effects of SLC9A3‑AS1 silencing on NPC cells were reversed by inhibiting miR‑486‑5p or overexpressing E2F6. In summary, SLC9A3‑AS1 exerted carcinogenic effects on NPC cells by adjusting the miR‑486‑5p/E2F6 axis. Accordingly, the newly identified SLC9A3‑AS1/miR‑486‑5p/E2F6 pathway may offer attractive therapeutic targets for future development.