The Long Noncoding RNA TUG1 Promotes Laryngeal Cancer Proliferation and Migration

• Main Authors: Zhonghua Zhang, Xuehai Wang, Shengda Cao, Xiao Han, Zhanwang Wang, Xiaoyan Zhao, Xuejun Liu, Guojun Li, Xinliang Pan, Dapeng Lei
• Format: Article
• Language: English
• Published: Cell Physiol Biochem Press GmbH & Co KG 2018-09-01
• Series: Cellular Physiology and Biochemistry
• Subjects: Long noncoding RNAs; TUG1; Laryngeal squamous cell carcinoma; proliferation; metastasis
• Online Access: https://www.karger.com/Article/FullText/493876

Background/Aims: Researchers have shown that long noncoding RNAs are closely associated with the pathogenesis of laryngeal squamous cell carcinoma (LSCC). However, the role of the long noncoding RNA taurine-upregulated gene 1 (TUG1) in the pathogenesis of LSCC remains unclear, although it is recognized as an oncogenic regulator for several types of squamous cell carcinoma. Methods: qRT-PCR was performed to measure the expression of TUG1 in LSCC tissues and cell lines. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) was used to measure the effect of TUG1 on cell proliferation. Transwell assay and flow cytometry were employed to determine the effect of TUG1 on cell migration and invasion. Western-blot were performed to explore the relation of TUG1 and p53 mRNA. Results: Higher TUG1 expression in LSCC than in paired normal tumor-adjacent tissue specimens (N = 64) was observed using quantitative real-time polymerase chain reaction. Also, high TUG1 expression was positively associated with advanced T category, worse lymph node metastasis and late clinical stage. Furthermore, in vitro experiments demonstrated that silencing of TUG1 markedly inhibited proliferation, cell-cycle progression, migration, and invasion of LSCC cells, whereas depletion of TUG1 led to increased apoptosis. Conclusion: These findings demonstrated that upregulated TUG1 expression exerted oncogenic effects by promoting proliferation, migration, and invasion, and inhibiting apoptosis in LSCC cells.