Network analysis of microRNAs, genes and their regulation in human bladder cancer

Abstract

Abstract. Bladder cancer (BC) is the fifth most common malignancy occurring worldwide and a significant cause of cancer-related morbidity and mortality. Although BC is a serious health issue, studies available concerning the relationship of genes, microRNAs (miRNAs) and their host genes has been lacking. In the present study, we assessed experimentally validated data from various sources that reported the effect of miRNA on various diseases, miRNA targeting of mRNAs, and combined these data with initial transcription factor (TF) binding site predictions within miRNA promoter regions. Topology networks obtained in this study included the differentially expressed, BC-associated and global networks. The three networks may be used to assess the effect of miRNAs and their regulation in human BC. By comparing and analyzing the similarities and differences among the three networks, key nodes with the largest potential of affecting the behavior of a particular network were identified. The results also showed potentially substantially influential miRNAs and TFs, which revealed subnetworks demonstrating the mechanisms involved as well as regulatory miRNA network motifs in human BC. Regulatory pathways regarding differentially expressed elements, such as genes and miRNAs, demonstrate self-adapting associations including, self-adapting associations and feedback loops in genes MYC, TP53, PTEN and 10 differentially expressed miRNAs. The differentially expressed network partially identified the BC mechanism. miRNA-targeted human BC genes were also enriched in highly relevant pathways, cell cycle regulation and apoptosis. The present study systematically delineated the pathogenesis of BC and provided theoretical foundations for gene therapy investigators to focu attention on key genes and miRNAs in future studies.

Inhibition of the LncRNA Gpr19 attenuates ischemia‐reperfusion injury after acute myocardial infarction by inhibiting apoptosis and oxidative stress via the miR‐324‐5p/Mtfr1 axis

“…MicroRNAs (miRNAs) are generally non‐protein‐coding RNAs of 20–22 nucleotides . They can bind and regulate the transcription or translation of mRNA and play biological roles in different diseases . Previous studies have shown that miR‐324‐5p can bind and inhibit Mtfr1 to alleviate I/R injury after MI .…”

“…23 They can bind and regulate the transcription or translation of mRNA and play biological roles in different diseases. 24,25 Previous studies have shown that miR-324-5p can bind and inhibit Mtfr1 to alleviate I/R injury after MI. 22 Through bioinformatics analysis, we confirmed that miR-324-5p could bind Mtfr1 in the 3 0 UTR.…”

The effect of inhibition of PP1 and TNFα signaling on pathogenesis of SARS coronavirus

“…Analysis of coexpression-type networks has been used previously to identify genes and proteins of increased importance to controlling system-wide host responses [10,[12][13][14][15]. The topological locations of genes in these networks can be used to identify hubs, genes that are connected to many other genes and therefore may be exerting a regulatory influence, and topological bottlenecks, genes that bridge disparate sub-networks and may serve as mediators of transitions between system states [16][17][18]. Recently, a node's participation in network motifs in directional networks was shown to be an effective predictor of importance [19].…”

MicroRNA‐410 promotes cell proliferation by targeting BRD7 in non‐small cell lung cancer

“…Increasing evidences show that aberrant expression of miRNAs plays significant roles in diverse biological processes such as development, differentiation, growth, and metabolism [13][14][15][16]. Meanwhile, deregulations of miRNAs are observed in a wide range of cancers, including breast cancer, gastric cancer, hepatocellular carcinoma, bladder cancer, osteosarcoma and glioblastoma [17][18][19][20][21][22][23]. MiRNAs can function either as tumor suppressor genes or oncogenes during tumor development and progression [23][24][25].…”