Zhang Zhonghua, Wang Xuehai, Cao Shengda, Han Xiao, Wang Zhanwang, Zhao Xiaoyan, Liu Xuejun, Li Guojun, Pan Xinliang, Lei Dapeng
Department of Otorhinolaryngology, Qilu Hospital, Shandong University, Key Laboratory of Otolaryngology, NHFPC (Shandong University), Jinan, China.
Department of Otorhinolaryngology, Weihai Municipal Hospital, Weihai, China.
Cell Physiol Biochem. 2018;49(6):2511-2520. doi: 10.1159/000493876. Epub 2018 Sep 27.
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.
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.
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.
These findings demonstrated that upregulated TUG1 expression exerted oncogenic effects by promoting proliferation, migration, and invasion, and inhibiting apoptosis in LSCC cells.
背景/目的:研究人员已表明长链非编码RNA与喉鳞状细胞癌(LSCC)的发病机制密切相关。然而,长链非编码RNA牛磺酸上调基因1(TUG1)在LSCC发病机制中的作用仍不清楚,尽管它被认为是几种类型鳞状细胞癌的致癌调节因子。
采用qRT-PCR检测TUG1在LSCC组织和细胞系中的表达。使用3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2-H-四氮唑溴盐(MTT)检测TUG1对细胞增殖的影响。采用Transwell实验和流式细胞术测定TUG1对细胞迁移和侵袭的影响。进行蛋白质免疫印迹法以探讨TUG1与p53 mRNA的关系。
使用定量实时聚合酶链反应观察到,LSCC中TUG1的表达高于配对的正常肿瘤旁组织标本(N = 64)。此外,TUG1高表达与T分期进展、更差的淋巴结转移和晚期临床分期呈正相关。此外,体外实验表明,沉默TUG1可显著抑制LSCC细胞的增殖、细胞周期进程、迁移和侵袭,而敲低TUG1则导致细胞凋亡增加。
这些发现表明,TUG1表达上调通过促进LSCC细胞的增殖、迁移和侵袭以及抑制细胞凋亡发挥致癌作用。