Department of Otolaryngology, Jining First People's Hospital of Shandong Province, Jining, Shandong, China.
Department of Otolaryngology, The Third People's Hospital of Qingdao, Qingdao, Shandong, China.
J Cell Biochem. 2019 Aug;120(8):13392-13402. doi: 10.1002/jcb.28614. Epub 2019 Mar 27.
Laryngocarcinoma is the most common head and neck cancer and has a high incidence and mortality, causing about 83 000 deaths per year worldwide. Our research aimed to investigate the possible role of long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) in laryngocarcinoma development. The messenger RNA (mRNA) levels of TUG1 in tumor tissues and control (plasma) samples of laryngocarcinoma patients as well as in laryngocarcinoma cells were detected. The influences of TUG1 suppression on cell biological processes (viability, apoptosis, migration, and invasion) and cytoskeleton rearrangement in laryngocarcinoma cells were tested. Moreover, we investigated the regulatory interaction between TUG1 and miR-145-5p, and identified the target gene of miR-145-5p. The association between TUG1 and the protein expressions of RhoA/rho associated coiled-coil containing protein kinase (ROCK)/matrix metalloproteinases (MMPs) pathway-associated factors were detected. TUG1 was found to be highly expressed in tumor tissues and plasma samples of laryngocarcinoma patients as well as in laryngocarcinoma cells. Suppression of TUG1 decreased laryngocarcinoma cell viability, increased apoptosis, and suppression migration, invasion, and cytoskeleton rearrangement. Moreover, TUG1 negatively regulated miR-145-5p. TUG1 regulated tumor growth (viability and apoptosis) and metastasis through miR-145-5p. Furthermore, ROCK1 was targeted by miR-145-5p, and miR-145-5p/ROCK1 partner was involved in the process of tumor growth and metastasis. Finally, we found that TUG1 functioned on laryngocarcinoma by activating RhoA/ROCK/MMPs pathway. Our study reveals that lncRNA TUG1 is upregulated in laryngocarcinoma and may be involved in the process of laryngocarcinoma through miR-145-5p downregulation and activating the RhoA/ROCK/MMPs signals.
喉癌是最常见的头颈部癌症，发病率和死亡率都很高，全世界每年约有 83000 人因此死亡。我们的研究旨在探讨长链非编码 RNA（lncRNA）牛磺酸上调基因 1（TUG1）在喉癌发展中的可能作用。检测了喉癌患者肿瘤组织和对照（血浆）样本以及喉癌细胞中的 TUG1 mRNA 水平。检测了 TUG1 抑制对喉癌细胞生物学过程（活力、凋亡、迁移和侵袭）和细胞骨架重排的影响。此外，我们研究了 TUG1 与 miR-145-5p 的调控相互作用，并鉴定了 miR-145-5p 的靶基因。检测了 TUG1 与 RhoA/rho 相关卷曲螺旋蛋白激酶（ROCK）/基质金属蛋白酶（MMPs）通路相关因子蛋白表达之间的关联。结果表明，TUG1 在肿瘤组织和喉癌患者血浆样本以及喉癌细胞中高表达。抑制 TUG1 降低了喉癌细胞活力，增加了细胞凋亡，并抑制了迁移、侵袭和细胞骨架重排。此外，TUG1 负调控 miR-145-5p。TUG1 通过 miR-145-5p 调节肿瘤生长（活力和凋亡）和转移。此外，ROCK1 是 miR-145-5p 的靶基因，miR-145-5p/ROCK1 对是肿瘤生长和转移过程中的重要因素。最后，我们发现 TUG1 通过激活 RhoA/ROCK/MMPs 信号通路作用于喉癌。本研究表明，lncRNA TUG1 在喉癌中上调，可能通过下调 miR-145-5p 并激活 RhoA/ROCK/MMPs 信号通路参与喉癌的发生。
