Pu Jian, Tan Chuan, Shao Zesheng, Wu Xianjian, Zhang Ya, Xu Zuoming, Wang Jianchu, Tang Qianli, Wei Huamei
Department of Hepatobiliary Surgery, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, People's Republic of China.
Graduate College, Youjiang Medical University for Nationalities, Baise, Guangxi, People's Republic of China.
Onco Targets Ther. 2020 Sep 16;13:9203-9211. doi: 10.2147/OTT.S259962. eCollection 2020.
In East Asia, hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancer types. Long noncoding RNA (lncRNA) prostate androgen-regulated transcript 1 () was reported to play crucial roles in regulating cancer progression. However, roles and mechanisms of action of in hepatocellular carcinoma (HCC) still remain unknown.
Quantitative real-time polymerase chain reaction (RT-qPCR) method was used to detect the expression level in HCC cells. Cell proliferation, colony formation, and transwell invasion assays were performed to investigate the biological roles of on HCC cell behaviors. Bioinformatic analysis methods were performed to analyze connections of microRNA-590-3p (miR-590-3p) with or high mobility group box 2 () in HCC. Moreover, expression levels of , miR-590-3p, and in HCC tissues and normal tissues were analyzed at ENCORI.
expression was found to be significantly upregulated in HCC tissues and cells. Functionally, silencing of significantly suppressed HCC cell proliferation, colony formation and invasion in vitro, while forcing exerts opposite biological effects. Mechanically, miR-590-3p/ axis was downstream target of , and silencing of miR-590-3p or forcing of could rescue the stimulation effects of overexpression on HCC cell behaviors.
Our results provided evidence that serves as oncogenic lncRNA through sponging miR-590-3p to upregulate expression in HCC.
在东亚地区，肝细胞癌（HCC）是最常被诊断出的癌症类型之一。据报道，长链非编码RNA（lncRNA）前列腺雄激素调节转录本1（ ）在调节癌症进展中起关键作用。然而， 在肝细胞癌（HCC）中的作用和作用机制仍不清楚。
采用定量实时聚合酶链反应（RT-qPCR）法检测HCC细胞中 的表达水平。进行细胞增殖、集落形成和Transwell侵袭试验，以研究 对HCC细胞行为的生物学作用。采用生物信息学分析方法分析微小RNA-590-3p（miR-590-3p）与HCC中 或高迁移率族蛋白盒2（ ）的联系。此外，在ENCORI分析了HCC组织和正常组织中 、miR-590-3p和 的表达水平。
发现 在HCC组织和细胞中显著上调。在功能上，沉默 显著抑制体外HCC细胞增殖、集落形成和侵袭，而强制表达 则产生相反的生物学效应。在机制上，miR-590-3p/ 轴是 的下游靶点，沉默miR-590-3p或强制表达 可挽救 过表达对HCC细胞行为的刺激作用。
我们的结果提供了证据，表明 通过海绵吸附miR-590-3p上调HCC中 的表达，从而作为致癌lncRNA。
