SNHG17 通过作为 microRNA-876 的竞争性内源性 RNA 发挥作用,从而增加特异性蛋白 1 的表达,增强舌鳞癌细胞的恶性特征。
SNHG17 enhances the malignant characteristics of tongue squamous cell carcinoma by acting as a competing endogenous RNA on microRNA-876 and thereby increasing specificity protein 1 expression.
机构信息
Institute of Oral Diseases, Oral Medicine Center, University of Chinese Academy of Sciences, Shenzhen Hospital, Shenzhen, Guangdong, P.R. China.
出版信息
Cell Cycle. 2020 Mar;19(6):711-725. doi: 10.1080/15384101.2020.1727399. Epub 2020 Feb 23.
A long noncoding RNA called (small nucleolar RNA host gene 17) is aberrantly expressed and plays essential roles in multiple human cancer types. Nevertheless, its expression pattern and specific functions in tongue squamous cell carcinoma (TSCC) have not been well studied until now. Hence, in this study, we aimed to measure expression in TSCC and to examine the actions of on the malignant characteristics of TSCC cells. The regulatory mechanism that mediates the oncogenic effects of on TSCC cells was investigated too. In this study, was found to be upregulated in TSCC, and this overexpression closely correlated with adverse clinical parameters and shorter overall survival among the patients with TSCC. The knockdown significantly decreased TSCC cell proliferation, migration, and invasion in vitro and tumor growth in vivo. Mechanism investigation revealed that acts as a competing endogenous RNA on microRNA-876 (miR-876) in TSCC cells. In addition, specificity protein 1 () was validated as a direct target gene of miR-876 in TSCC cells. SP1 expression restoration in TSCC cells reversed miR-876 overexpression-induced anticancer effects. MiR-876 downregulation strongly attenuated the actions of the knockdown in TSCC cells. plays an oncogenic part in TSCC cells both in vitro and in vivo via sponging of miR-876 and thereby upregulating SP1, which could be regarded as a promising target for TSCC therapy.
一种称为 (小核仁 RNA 宿主基因 17)的长非编码 RNA 表达异常,在多种人类癌症类型中发挥重要作用。然而,直到现在,其在舌鳞状细胞癌(TSCC)中的表达模式和特定功能仍未得到很好的研究。因此,在这项研究中,我们旨在测量 TSCC 中的 表达,并研究 对 TSCC 细胞恶性特征的作用。还研究了介导 对 TSCC 细胞致癌作用的调节机制。在这项研究中,发现 在 TSCC 中上调,这种过表达与 TSCC 患者的不良临床参数和总体生存率缩短密切相关。 在体外显著降低了 TSCC 细胞的增殖、迁移和侵袭,并且在体内降低了肿瘤生长。机制研究表明, 在 TSCC 细胞中作为 microRNA-876 (miR-876) 的竞争性内源 RNA 发挥作用。此外,特异性蛋白 1 () 被验证为 TSCC 细胞中 miR-876 的直接靶基因。在 TSCC 细胞中恢复 SP1 表达逆转了 miR-876 过表达诱导的抗癌作用。在 TSCC 细胞中下调 miR-876 可显著减弱 的敲低作用。 通过海绵吸附 miR-876 并上调 SP1, 在体外和体内均在 TSCC 细胞中发挥致癌作用,可视为 TSCC 治疗的有前途的靶点。