Long non-coding RNA SLC16A1-AS1: its multiple tumorigenesis features and regulatory role in cell cycle in oral squamous cell carcinoma

• Published in: Cell cycle (Georgetown, Tex.) Vol. 19; no. 13; pp. 1641 - 1653
• Main Authors: Feng, Hao, Zhang, Xiaoqi, Lai, Wenli, Wang, Jian
• Format: Journal Article
• Language: English
• Published: United States Taylor & Francis 02.07.2020
• Subjects: bioinformatics; cell cycle; lncRNA SLC16A1-AS1; Oral squamous cell carcinoma; Research Paper; tumorigenesis; Oral squamous cell carcinoma; tumorigenesis; cell cycle; lncRNA SLC16A1-AS1; bioinformatics
• ISSN: 1538-4101; 1551-4005
• DOI: 10.1080/15384101.2020.1762048

Altered expressions of long non-coding RNAs (lncRNAs) are potential cancer prognostic biomarkers that play a critical role in the development of tumorigenesis and metastasis of cancer. However, the relationship between the expression of lncRNAs in oral squamous cell carcinoma (OSCC) and the diagnosis, progression, and prognosis of OSCC has not been thoroughly elucidated. To identify the differentially expressed lncRNAs between OSCC tissue and normal tissue, RNA-Seq data were used. lncRNA SLC16A1-AS1 was significantly highly expressed in OSCC samples than that in normal samples. Systematic bioinformatics analysis revealed that SLC16A1-AS1 was associated with histological tumor grades and overall survival status, as well as copy number variation, somatic mutation, tumor mutation burden, tumor stemness, tumor microenvironment and infiltrating immune cells. According to three advanced bioinformatic algorithms prediction (WGCNA, GSEA and GSVA), SLC16A1-AS1 played an essential role in OSCC proliferation and its biological function was related to cell-cycle regulation. Loss-of-function experiments were performed to determine the biological functions of SLC16A1-AS in OSCC cells. Silencing SLC16A1-AS1 significantly reduced the cell proliferation rate and colony-forming ability in both CAL27 and SCC25 cell lines. Flow cytometry and western blot analysis revealed that SLC16A1-AS1 silencing induced G0/G1 cell cycle arrest and inhibited the expression of cyclin D1 in both CAL27 and SCC25 cells. In conclusion, our study comprehensively investigated the role of the lncRNA SLC16A1-AS1 in OSCC growth and proved that it may serve as a new diagnostic indicator and a new target for the treatment of OSCC.