Yuan Shouxian, Luan Xiuhua, Chen Haixia, Shi Xiuqing, Zhang Xiangkai
Department of Urology Surgery, The Second People's Hospital of Liaocheng, Linqing, Shandong 252600, P.R. China.
Department of Medical Records, The Second People's Hospital of Liaocheng, Linqing, Shandong 252600, P.R. China.
Oncol Lett. 2020 Mar;19(3):1899-1905. doi: 10.3892/ol.2020.11283. Epub 2020 Jan 9.
The present study aimed to investigate the role of the long non-coding RNA EGFR-AS1 in bladder cancer (BC). In this study gene expression of both BC and non-tumor tissues from BC patients were measured by quantitative PCR. Cell transfections were performed to analyze gene interactions in HT-1197 cells. Transwell assays were performed to analyze cell invasion and migration of HT-1197 cells. It was revealed that epidermal growth factor receptor-antisense RNA 1 (EGFR-AS1) was upregulated in BC and positively associated with rho associated coiled-coil containing protein kinase 2 (ROCK2). Analysis of data collected in follow-ups indicated that EGFR-AS1 expression was significantly associated with poorer overall survival of patients with BC. Moreover, in bladder cancer cells, EGFR-AS1 overexpression mediated the upregulation of ROCK2, while microRNA (miR)-381 mediated the downregulation of ROCK2. However, EGFR-AS1 and ROCK2 failed to affect each other. Bioinformatics analysis indicated that miR-381 binds EGFR-AS1. In addition, EGFR-AS1 and ROCK2 overexpression resulted in the promotion of cell invasiveness and migration of HT-1197 BC cells. Conversely, miR-381 was revealed to partially reverse the effect of EGFR-AS1 overexpression. Therefore, EGFR-AS1 may sponge miR-381 to upregulate ROCK2 in BC, thereby promoting cell invasion and migration.
本研究旨在探讨长链非编码RNA表皮生长因子受体反义RNA1(EGFR-AS1)在膀胱癌(BC)中的作用。在本研究中,通过定量PCR检测了BC患者的BC组织和非肿瘤组织的基因表达。进行细胞转染以分析HT-1197细胞中的基因相互作用。进行Transwell实验以分析HT-1197细胞的侵袭和迁移。结果显示,表皮生长因子受体反义RNA1(EGFR-AS1)在BC中上调,并与含rho相关卷曲螺旋蛋白激酶2(ROCK2)呈正相关。随访收集的数据分析表明,EGFR-AS1表达与BC患者较差的总生存期显著相关。此外,在膀胱癌细胞中,EGFR-AS1过表达介导了ROCK2的上调,而微小RNA(miR)-381介导了ROCK2的下调。然而,EGFR-AS1和ROCK2未能相互影响。生物信息学分析表明,miR-381与EGFR-AS1结合。此外,EGFR-AS1和ROCK2过表达导致HT-1197 BC细胞的侵袭性和迁移增加。相反,miR-381被发现可部分逆转EGFR-AS1过表达的作用。因此,EGFR-AS1可能通过吸附miR-381上调BC中的ROCK2,从而促进细胞侵袭和迁移。