ArticleBiochemical genetics2023
Long Non-Coding RNA Small Nucleolar RNA Host Gene 4 Induced by Transcription Factor SP1 Promoted the Progression of Nasopharyngeal Carcinoma Through Modulating microRNA-510-5p/Centromere Protein F Axis.
Article in Biochemical genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Centromere Protein F in Tumor Biology: Cancer's Achilles Heel.Cancer medicine · 2025Review
- Long noncoding RNA SNHG4 promotes glioma progression via regulating miR-367-3p/MYO1B axis in zebrafish xenografts.Human cell · 2025Article
- lncRNAs are potential prognostic markers in patients with nasopharyngeal carcinoma in China: A systematic review and meta‑analysis.Molecular and clinical oncology · 2024Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (LncRNAs) are implicated with tumorigenesis and the development of nasopharyngeal carcinoma (NPC). Previous studies suggested that long non-coding RNA small nucleolar RNA host gene 4 (SNHG4) exerted oncogenic roles in various cancers. However, the function and molecular mechanism of SNHG4 in NPC have not been investigated. In our study, it was confirmed that the SNHG4 level was enriched in NPC tissues and cells. Functional assays indicated that SNHG4 depletion inhibited the proliferation and metastasis but promoted apoptosis of NPC cells. Furthermore, we identified miR-510-5p as a downstream gene of SNHG4 in NPC cells and SNHG4 upregulated CENPF expression by binding to miR-510-5p. Moreover, there was a positive (or negative) association between CENPF and SNHG4 (or miR-510-5p) expression in NPC. In addition, rescue experiments verified that CENPF overexpression or miR-510-5p silencing abrogated inhibitory effects on NPC tumorigenesis caused by SNHG4 deficiency. The study demonstrated that SNHG4 promoted NPC progression via miR-510-5p/CENPF axis, providing a novel potential therapeutic target for NPC treatments.
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Registered trials
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