Small nucleolar RNA host gene 3 facilitates cell proliferation and migration in oral squamous cell carcinoma via targeting nuclear transcription factor Y subunit gamma.

Abstract

Oral squamous cell carcinoma (OSCC) has been reported to be the most common oral carcinoma. Emerging evidence has revealed the key role that long noncoding RNAs (lncRNAs) play in numerous malignancies, including OSCC. LncRNA small nucleolar RNA host gene 3 (SNHG3) has been reported as an oncogenic factor in some cancers. Nonetheless, the role of SNHG3 in OSCC has never been clarified. In this study, we analyzed the expression patterns of SNHG3 in OSCC through quantitative real-time polymerase chain reaction. It was revealed that the expression level of SNHG3 was remarkably elevated in OSCC cell lines compared with the nontumor cell line. It was demonstrated by functional experiments that SNHG3 knockdown notably inhibited cell proliferation and migration in OSCC. RNA immunoprecipitation, RNA pull down, and messenger RNA (mRNA) stability test verified that SNHG3 decoyed ELAV like RNA-binding protein 1 (ELAVL1) and therefore stabilized nuclear transcription factor Y subunit gamma (NFYC) mRNA to upregulate the expression levels of NFYC in OSCC cells. At last, it was confirmed by rescue experiments that the inhibiting impacts of SNHG3 knockdown on OSCC cell proliferation and migration could be partly revived by NFYC overexpression. Besides, we validated that Wnt/β-catenin pathway was also involved in SNHG3-regulated OSCC progression. In conclusion, SNHG3 might serve as a novel biomarker for OSCC.