Critical miRNAs as a Biomarker in Development and Progression of Rhabdomyosarcoma

Abstract

AbstractRhabdomyosarcoma (RMS) is the most prevalent pediatric soft tissue malignancy. The early metastasis and recurrence of RMS, as well as the pain and bleeding induced by tumor compression, significantly compromise therapy efficacy and prognosis. In some cases, up to 37.7 percent of RMS spread to other parts of the body. Therefore, it is important to investigate the molecular pathways behind RMS in order to find a reliable target for the early detection and targeted treatment of this cancer. A microarray dataset of 63 RMS tissue samples and 63 control group samples was obtained and analyzed. GEO2R was able to detect genes that were differentially expressed miRNAs between rhabdomyosarcoma and normal tissue. Analysis of gene ontology ( molecular functions and biological processes) and the Kyoto Encyclopedia of Genes and Genomes pathways was conducted. Hub target genes of miRNAs were found through building an interaction network. Then we intersection between miRNAs RMS profile and miRnone of RMS. In RMS tumor tissues, 75 miRNAs were found to be up-regulated and 86 miRNAs were found to be down-regulated. According to the results of the gene ontology analysis, the functions of the cell cycle, retinal pigmented epithelium development, oxidative stress, cellular aging, and PI3K/AKT were the most significantly enriched. With 75 nodes and 1740 edges, hsa-miR-758-3p, hsa-miR-1908-3p, hsa-miR-127-5p and hsa-miR-6762-3p upregulated miRNAs and hsa-miR-1229-5p, hsa-miR-6831-5p, hsa-miR-4660, hsa-miR-3908, hsa-miR-1182, hsa-miR-6796-5p, hsa-miR-1180-3p, hsa-miR-519e-3p and hsa-miR-370-5p downregulated miRNAs were observed with miRnome of RMS. hsa-miR-410-3p were possibility role to invasion RMS tumor to retina. Our results show that RMS and normal tissue samples had varied miRNAs expression levels. As hsa-miR-410-3p and hsa-miR-127-5p have been hypothesized to play a role in the etiology of RMS, they should be studied in greater depth.