PRR11 is a prognostic biomarker and correlates with immune infiltrates in bladder urothelial carcinoma

• Published in: Scientific reports Vol. 13; no. 1; p. 2051
• Main Authors: Ni, Wenpeng, Yi, Lijuan, Dong, Xiaoru, Cao, Mengjie, Zheng, Jinjuan, Wei, Qingling, Yuan, Chunlei
• Format: Journal Article
• Language: English
• Published: England Nature Publishing Group 04.02.2023; Nature Publishing Group UK; Nature Portfolio
• Subjects: Bioinformatics; Biomarkers; Bladder cancer; Carcinoma, Transitional Cell; Gene expression; Genomes; Humans; Immunotherapy; Infiltration; Metastases; Microsatellite instability; Prognosis; Tumor microenvironment; Tumor Microenvironment - genetics; Tumors; Urinary Bladder; Urinary Bladder Neoplasms - genetics; Urothelial carcinoma
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-023-29316-2

Abnormal proline-rich protein 11 (PRR11) expression is associated with various tumors. However, there are few reports concerning PRR11 with prognostic risk, immune infiltration, or immunotherapy of bladder urothelial carcinoma (BLCA). This study is based on online databases, such as Oncomine, GEPIA, HPA, LinkedOmics, TIMER, ESTIMATE and TISIDB, and BLCA data downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus, we employed an array of bioinformatics methods to explore the potential oncogenic roles of PRR11, including analyzing the relationship between PRR11 and prognosis, tumor mutational burden (TMB), microsatellite instability, and immune cell infiltration in BLCA. The results depict that PRR11 is highly expressed in BLCA, and BLCA patients with higher PRR11 expression have worse outcomes. In addition, there was a significant correlation between PRR11 expression and TMB and tumor immune infiltration. These findings suggest that PRR11 can be used as a potential marker for BLCA patient assessment and risk stratification to improve clinical prognosis, and its potential regulatory mechanism in the BLCA tumor microenvironment and targeted therapy is worthy of further investigation.