IL1RL2 is related to the expression and prognosis of bladder cancer

IL1RL2与膀胱癌的表达及预后相关

阅读:5
作者:Xuemei Ha, Yue Li, Zihui Gao, Jiazhao Cui, Yuzhu Nie, Lihua Sun, Wenzhi Gao

Abstract

IL1RL2 has been reported to be highly expressed in a variety of tumor types whereas its role in bladder cancer (BLCA) remains unclear. The aim of the present study was to explore the prognostic value of Il1RL2 in BLCA and its relationship with clinical pathological features. The Cancer Genome Atlas (TCGA) database was used to assess the levels of IL1RL2 expression in BLCA tissues and cells, which were validated by reverse transcription-quantitative polymerase chain reaction and western blotting. Immunohistochemistry was employed to analyze expression of the IL1RL2 gene in 17 pairs of tumor and normal specimens, as well as 112 samples with different stages and grades of tumors. To investigate the biological functions of Il1RL2 in BLCA, co-expression networks and functional enrichment analyses were conducted. A protein-protein interaction network was constructed using interaction gene search tools. IL1RL2 was revealed to be clearly expressed in BLCA cells and tissues. The area under the curve for amplification of IL1RL2 distinguishing between tumor and normal tissues was 0.700 (95% CI: 0.579-0.821) in the TCGA database and 0.647 (95% CI: 0.497-0.797) in Miyun chart database, respectively. Furthermore, in our database, both univariate and multivariate analyses indicated that IL1RL2 expression was an independent risk factor for overall survival (OS). Kaplan-Meier survival analysis revealed an association between high IL1RL2 expression and low OS. Pathway enrichment analysis suggested that IL1RL2 is involved in the regulation of tumor progression through the MAPK signaling pathway. The expression level of IL1RL2 was associated with the stage, grade, lymph node album and prognosis of BLCA.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。