Breast cancer is the second leading cause of cancer-associated mortality among women worldwide, and the prevalence and mortality rates associated with this disease are high in Western countries. The melanoma-associated antigen (MAGE) family proteins are well-known tumor-specific antigens; this family includes >60 proteins that serve an important part in cell cycle withdrawal, neuronal differentiation and apoptosis. The aim of the present study was to identify a biomarker within the MAGE family that is specific for breast cancer. In the present study, the prognostic role of MAGE mRNA expression was investigated in patients with breast cancer using the Kaplan-Meier plotter database. The prognostic value of MAGE members in the different intrinsic subtypes of breast cancer was further investigated, as well as the clinicopathological features of the disease. The results of the present study indicated that patients with breast cancer that had high mRNA expression levels of MAGEA5, MAGEA8, MAGEB4 and MAGEB6 had an improved relapse-free survival, whereas those with high mRNA expression levels of MAGEB18 and MAGED4 did not. These results suggested that MAGEA5, MAGEA8, MAGEB4 and MAGEB6 may have roles as tumor suppressors in the occurrence and development of breast cancer, whereas MAGEB18 and MAGED4 may possess carcinogenic potential. MAGED2, MAGED3 and MAGEF1 had different effects depending on the type of breast cancer. In particular, high MAGEC3 mRNA expression was associated with worse RFS in lymph node-positive breast cancer, but with improved RFS in lymph node-negative breast cancer. In patients with wild-type TP53 and patients with different pathological grades of breast cancer, MAGEE2, MAGEH1 and MAGEL2 were more worthy of attention as potential prognostic factors. The results of the present study may help to elucidate the role of MAGE family members in the development of breast cancer, and may promote further research that identifies MAGE-targeting reagents for the treatment of breast cancer.
Introduction: Prostate adenocarcinoma is one of the most prevalent causes of cancer-related deaths in males worldwide. However, the underlying mechanisms remain poorly understood. Hence, it is important to identify specific and effective therapeutic targets, to be able to determine appropriate therapy and management. So, this study aimed to predict that miR-93-5p is an important oncogene in prostate cancer by bioinformatics analysis. Methods: In this study, initially we identified differentially expressed genes (DEGs) and differently expressed miRNAs (DEMs) in the The Cancer Genome Atlas (TCGA) database, performed Gene Ontology (GO) and pathway enrichment analysis, then investigated the relationship between DEGs and DEMs, and finally through consulting the literature and retrieving the database, we found that miR-93-5p may play a major role in prostate cancer, so we predicted the expression and survival of miR-93-5p and its isomers by bioinformatics analysis, meanwhile, evaluated the function of miR-93-5p in vitro. Results: In total, 104 DEMs were differently expressed between prostate cancer and normal samples, including 56 downregulated ones and 48 upregulated ones; miR-93-5p (upregulated) was identified as a good biomarker. And 1904 DEGs were retrieved, including 794 downregulated ones and 1110 upregulated ones. We also obtained 1254 DEGs of the DEMs. In GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, the significantly enriched pathways involved pathway in focal adhesion, vascular smooth muscle contraction, and regulation of actin cytoskeleton. By the KEGG pathway, we got 16 target genes and 92 pathways of the miR-93-5p in prostate cancer. We also found that the miR-93-5p and its isomers can express in prostate cancer, and which with a high expression had a poor overall survival and a significant difference recurrence rate within 5 years. Further in vitro verification results demonstrated that the low expression of miR-93-5p can inhibit cell proliferation, migration, invasion, change cell cycle, and promote early apoptosis of PC-3 cells. Conclusion:The miR-93-5p and its target genes were used to define important molecular targets that could serve as a prognostic and predictive marker in the
Background Though considerable efforts have been made to improve the treatment of epithelial ovarian cancer (EOC), the prognosis of patients has remained poor. Identifying differentially expressed genes (DEGs) involved in EOC progression and exploiting them as novel biomarkers or therapeutic targets is of great value. Methods Overlapping DEGs were screened out from three independent gene expression omnibus (GEO) datasets and were subjected to Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analyses. The protein-protein interactions (PPI) network of DEGs was constructed based on the STRING database. The expression of hub genes was validated in GEPIA and GEO. The relationship of hub genes expression with tumor stage and overall survival and progression-free survival of EOC patients was investigated using the cancer genome atlas data. Results A total of 306 DEGs were identified, including 265 up-regulated and 41 down-regulated. Through PPI network analysis, the top 20 genes were screened out, among which 4 hub genes, which were not researched in depth so far, were selected after literature retrieval, including CDC45, CDCA5, KIF4A, ESPL1. The four genes were up-regulated in EOC tissues compared with normal tissues, but their expression decreased gradually with the continuous progression of EOC. Survival curves illustrated that patients with a lower level of CDCA5 and ESPL1 had better overall survival and progression-free survival statistically. Conclusion Two hub genes, CDCA5 and ESPL1, identified as probably playing tumor-promotive roles, have great potential to be utilized as novel therapeutic targets for EOC treatment.
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