The present study aimed to identify
bladder cancer-associated
microRNAs (
miRNAs) and target genes, and further analyze the potential molecular mechanisms involved in
bladder cancer. The
mRNA and
miRNA expression profiling dataset GSE40355 was downloaded from the Gene Expression Omnibus database. The Limma package in R was used to identify differential expression levels. The Human
microRNA Disease Database was used to identify
bladder cancer-associated
miRNAs and Target prediction programs were used to screen for
miRNA target genes. Enrichment analysis was performed to identify biological functions. The Database for Annotation, Visualization and Integration Discovery was used to perform OMIM_DISEASE analysis, and then
protein-
protein interaction (PPI) analysis was performed to identify hubs with biological essentiality. ClusterONE plugins in cytoscape were used to screen modules and the InterPro database was used to perform protein domain enrichment analysis. A group of 573 disease dysregulated genes were identified in the present study. Enrichment analysis indicated that the muscle organ development and vascular smooth muscle contraction pathways were significantly enriched in terms of disease dysregulated genes.
miRNAs targets (frizzled class receptor 8, EYA transcriptional coactivator and
phosphatase 4, sacsin
molecular chaperone,
calcium voltage-gated channel auxiliary subunit β2,
peptidase inhibitor 15 and
catenin α2) were mostly associated with
bladder cancer. PPI analysis revealed that
calmodulin 1 (CALM1), Jun proto-oncogene,
AP-1 transcription factor subunit (JUN) and
insulin like growth factor 1 (IGF1) were the important hub nodes. Additionally, protein domain enrichment analysis indicated that the
serine/threonine protein kinase active site was enriched in module 1 extracted from the PPI network. Overall, the results suggested that the IGF signaling pathway and RAS/
MEK/
extracellular signal-regulated kinase transduction signaling may exert vital molecular mechanisms in
bladder cancer, and that CALM1, JUN and IGF1 may be used as novel potential therapeutic targets.