The tumor microenvironment (TME) has been a major focus of research in recent years as a crucial factor in the development and progression of
bladder cancer. Unfortunately, the precise composition of TME, particularly the immunological and stromal components, remains unknown. In this work, we downloaded the
RNA-seq expression profiles and somatic mutation data of 433
bladder cancer cases from The
Cancer Genome Atlas (TCGA) and then employed a comprehensive bioinformatics approach to evaluate them. Firstly, the expression profiles were used to predict the scores and then the content of immune and stromal cells via the estimate package in R software. We then identified differentially expressed genes (DEGs) and differentially mutated genes (DMGs) according to the high-stromal score cohort and low-stromal score cohort. Finally,
fibroblast growth factor receptor 3 (FGFR3) was the main differentially mutated gene in bladder
carcinoma that we discovered after conducting a cross-study on DEGs and DMGs. Follow-up investigation revealed that FGFR3, whose expression correlated inversely with
cancer progression stage, appeared to be a protective factor in
bladder cancer. The method of Gene Set Enrichment Analysis (GSEA) was employed to, respectively, interpret the expression data of FGFR3 in high and low expression lists. We observed that the genes in the low FGFR3 expression list were strongly enriched in the biological processes associated with
transplantation and cell adhesion, suggesting the possible role of FGFR3 in predicting TME
metastasis status in
bladder cancer. Therefore, this study is aimed at investigating whether FGFR3 is promising as a
biomarker of TME remodeling to explain underlying mechanisms involved in
tumorigenesis and
metastasis, which may help to make decisions on treatments for
bladder cancer.