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Overexpressed circPVT1 in oral squamous cell carcinoma promotes proliferation by serving as a miRNA sponge

Circular RNAs (circRNAs) comprise a novel class of widespread non-coding RNAs that may regulate gene expression in eukaryotes. However, the characterization and function of circRNAs remain elusive in human cancer, including oral squamous cell carcinoma (OSCC). In this study, the expression level of...

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Detalles Bibliográficos
Autores principales: He, Tianpeng, Li, Xin, Xie, Dongmei, Tian, Lili
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6755181/
https://www.ncbi.nlm.nih.gov/pubmed/31485648
http://dx.doi.org/10.3892/mmr.2019.10615
Descripción
Sumario:Circular RNAs (circRNAs) comprise a novel class of widespread non-coding RNAs that may regulate gene expression in eukaryotes. However, the characterization and function of circRNAs remain elusive in human cancer, including oral squamous cell carcinoma (OSCC). In this study, the expression level of circPVT1 in OSCC was detected and define its functional role in initiation and progression of OSCC. It was identified that circPVT1 was upregulated in OSCC cells and specimens. Knockdown of circPVT1 suppressed cell proliferation as evidenced by Cell Counting kit-8 assay and elevated Ki-67 expression. Mechanistically, it was demonstrated that circPVT1 possessed two targeting sites of microRNA (miRNA/miR)-125b and could effectively sponge miR-125b to release its downstream mRNA targets. Subsequently, the downstream target signal transducer and activator of transcription 3 (STAT3) was verified as a direct target of miR-125b and STAT3 expression was regulated by the circPVT1/miR-125b axis. CircPVT1 functioned as competing endogenous RNA (ceRNA) to increase the STAT3 level and cell proliferation through sponging miR-125b. In conclusion, circPVT1 regulates cell proliferation and may serve as a promising therapeutic target for OSCC patients. Therefore, silencing of circPVT1 could be a future direction to develop a novel treatment strategy.