FBXL19‑AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR‑431 and upregulate PBOV1

Dong,Hongjun; Huang,Chao; Huang,Jingjing

doi:10.3892/mmr.2021.12286

FBXL19‑AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR‑431 and upregulate PBOV1

Authors:
- Hongjun Dong
- Chao Huang
- Jingjing Huang
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Affiliations: Department of Otorhinolaryngology, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Zhangjiagang, Jiangsu 215600, P.R. China
Published online on: July 12, 2021 https://doi.org/10.3892/mmr.2021.12286
Article Number: 647
Copyright: © Dong et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Long non‑coding RNAs (lncRNAs) have been shown to function as crucial regulators in the progression of various types of cancer, including nasopharyngeal carcinoma (NPC). The aim of the present study was to investigate the mechanisms underlying the role of the FBXL19‑AS1/microRNA (miR)‑431/prostate and breast cancer overexpressed 1 (PBOV1) axis in the progression of NPC. The expression levels of FBXL19‑AS1, miR‑431 and PBOV1 were assessed by reverse transcription‑quantitative PCR. The Cell Counting Kit‑8 assay was utilized to detect cell viability. Cell migration and invasion were determined using a Transwell assay. The associations between FBXL19‑AS1 and miR‑431 or miR‑431 and PBOV1 were verified via bioinformatics analysis, dual‑luciferase and RNA‑binding protein immunoprecipitation assays. It was demonstrated that the expression levels of FBXL19‑AS1 and PBOV1 were upregulated in NPC tissues and cells, whereas miR‑431 expression was downregulated. FBXL19‑AS1 directly interacted with miR‑431. FBXL19‑AS1 silencing inhibited the viability, migration and invasion of C666‑1 and SUNE1 cells, whereas these effects could be alleviated by suppressing miR‑431. miR‑431 could target the 3'‑untranslated region of PBOV1. Overexpression of PBOV1 neutralized the miR‑431‑mediated suppression of NPC progression. Moreover, FBXL19‑AS1 could regulate PBOV1 by sponging miR‑431 in NPC cells. In conclusion, the lncRNA FBXL19‑AS1 accelerated NPC progression via the miR‑431/PBOV1 axis, suggesting that it may serve as a potential therapeutic target for patients with NPC.

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