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

  • Authors:
    • Jiansheng Li
    • Dongzhi Li
    • Xianhua Zhang
    • Cuijuan Li
    • Fengjuan Zhu
  • View Affiliations / Copyright

    Affiliations: Department of Otolaryngology, The People's Hospital of Rizhao, Rizhao, Shandong 276826, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 165
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    Published online on: June 17, 2021
       https://doi.org/10.3892/or.2021.8116
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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.
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Copy and paste a formatted citation
Spandidos Publications style
Li J, Li D, Zhang X, Li C and Zhu F: Long noncoding RNA SLC9A3‑AS1 increases E2F6 expression by sponging microRNA‑486‑5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma. Oncol Rep 46: 165, 2021.
APA
Li, J., Li, D., Zhang, X., Li, C., & Zhu, F. (2021). Long noncoding RNA SLC9A3‑AS1 increases E2F6 expression by sponging microRNA‑486‑5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma. Oncology Reports, 46, 165. https://doi.org/10.3892/or.2021.8116
MLA
Li, J., Li, D., Zhang, X., Li, C., Zhu, F."Long noncoding RNA SLC9A3‑AS1 increases E2F6 expression by sponging microRNA‑486‑5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma". Oncology Reports 46.2 (2021): 165.
Chicago
Li, J., Li, D., Zhang, X., Li, C., Zhu, F."Long noncoding RNA SLC9A3‑AS1 increases E2F6 expression by sponging microRNA‑486‑5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma". Oncology Reports 46, no. 2 (2021): 165. https://doi.org/10.3892/or.2021.8116
Copy and paste a formatted citation
x
Spandidos Publications style
Li J, Li D, Zhang X, Li C and Zhu F: Long noncoding RNA SLC9A3‑AS1 increases E2F6 expression by sponging microRNA‑486‑5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma. Oncol Rep 46: 165, 2021.
APA
Li, J., Li, D., Zhang, X., Li, C., & Zhu, F. (2021). Long noncoding RNA SLC9A3‑AS1 increases E2F6 expression by sponging microRNA‑486‑5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma. Oncology Reports, 46, 165. https://doi.org/10.3892/or.2021.8116
MLA
Li, J., Li, D., Zhang, X., Li, C., Zhu, F."Long noncoding RNA SLC9A3‑AS1 increases E2F6 expression by sponging microRNA‑486‑5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma". Oncology Reports 46.2 (2021): 165.
Chicago
Li, J., Li, D., Zhang, X., Li, C., Zhu, F."Long noncoding RNA SLC9A3‑AS1 increases E2F6 expression by sponging microRNA‑486‑5p and thus facilitates the oncogenesis of nasopharyngeal carcinoma". Oncology Reports 46, no. 2 (2021): 165. https://doi.org/10.3892/or.2021.8116
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