ArticleMolecular medicine reports2021
FBXL19‑AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR‑431 and upregulate PBOV1.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- MicroRNA Binding Site Polymorphisms in Hepatocellular Carcinoma: Implications for Pathogenesis, Prognosis, and Therapeutic Response.International journal of genomics · 2025Review
- FLVCR1-AS1 and FBXL19-AS1: Two Putative lncRNA Candidates in Multiple Human Cancers.Non-coding RNA · 2022Review
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3 authors at 1 institution in 1 country.
Funding
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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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