Long noncoding RNA SLC9A3-AS1 increases E2F6 expression by sponging microRNA-486-5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma

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.