ABSTRACT
Background: Colorectal cancer [CRC] is one of the challenging types of cancers; thus, exploring effective biomarkers related to colorectal could lead to significant progresses toward the treatment of this disease
Methods: In the present study, CRC gene expression datasets have been reanalyzed. Mutual differentially expressed genes across 294 normal mucosa and adjacent tumoral samples were then utilized in order to build two independent transcriptional regulatory networks. By analyzing the networks topologically, genes with differential global connectivity related to cancer state were determined for which the potential transcriptional regulators including transcription factors were identified
Results: The majority of differentially connected genes [DCGs] were up-regulated in colorectal transcriptome experiments. Moreover, a number of these genes have been experimentally validated as cancer or CRC-associated genes. The DCGs, including GART, TGFB1, ITGA2, SLC16A5, SOX9, and MMP7, were investigated across 12 cancer types. Functional enrichment analysis followed by detailed data mining exhibited that these candidate genes could be related to CRC by mediating in metastatic cascade in addition to shared pathways with 12 cancer types by triggering the inflammatory events
Conclusion: Our study uncovered correlated alterations in gene expression related to CRC susceptibility and progression that the potent candidate biomarkers could provide a link to disease
ABSTRACT
Background: Crohn's disease is the most challenging, common type of autoimmune disorders due to which, intestine is inflamed but its causes have not been defined. Although Crohn's disease has been often thought of as an autoimmune disorder, it can be triggered by whatever that lead to the inflammation in the whole bowel. Henceforth, exploring trade-off among this disease and genomic variants supposedly will enhance the identification of important genes and in turn to the possible therapeutic protocols. The aim of the present study was to identify any association between Crohn's disease and single nucleotide polymorphisms.
Materials and methods: We retrieved single nucleotide polymorphism of genome-wide association studies [GWAS] on Crohn's disease among which we extracted neighboring genes and expression variants in addition to pathways in which the affected genes are enriched.
Results: Using GWAS data can help to explain the disease incidence. We noticed that genes harboring single nucleotide polymorphisms in Crohn's disease were mainly enriched in interleukin pathways in addition to fatty acid and choline metabolism.
Conclusion: The affected genes obtained by data analysis like fatty acid desaturase [FADS] and solute carrier family 22 [SLC22] could be proposed for future studies in order to clarifying their interactions by confident experiments and cross-sectional studies
ABSTRACT
Background: Alzheimer's Disease [AD] is the most common form of dementia in the elderly. Due to the facts that biological causes of AD are complex in addition to increasing rates of AD worldwide, a deeper understanding of AD etiology is required for AD treatment and diagnosis
Methods: To identify molecular pathological alterations in AD brains, GSE36980 series containing microarray data samples from temporal cortex, frontal cortex and hippocampus were downloaded from Gene Expression Omnibus [GEO] database and valid gene symbols were subjected to building a gene co-expression network by a bioinformatics tool known as differential regulation from differential co-expression [DCGL] software package. Then, a network-driven integrative analysis was performed to find significant genes and underlying biological terms
Results: A total of 17088 unique genes were parsed into three independent differential co-expression networks. As a result, a small number of differentially co-regulated genes mostly in frontal and hippocampus lobs were detected as potential biomarkers related to AD brains. Ultimately differentially co-regulated genes were enriched in biological terms including response to lipid and fatty acid and pathways mainly signaling pathway such as G-protein signaling pathway and glutamate receptor groups II and III. By conducting co-expression analysis, our study identified multiple genes that may play an important role in the pathogenesis of AD
Conclusion: The study aimed to provide a systematic understanding of the potential relationships among these genes and it is hoped that it could aid in AD biomarker discovery
ABSTRACT
Aim: we mainly aimed to elucidate potential comorbidities between celiac disease and hepatitis c by means of data and network analysis approaches
Background: understanding the association among the disorders evidently has important impact on the diagnosis and therapeutic approaches. Celiac disease is the most challenging, common types of autoimmune disorders. On the other hand, hepatitis c virus genome products like some proteins are supposed to be resemble to gliadin types that in turn activates gluten intolerance in people with inclined to gluten susceptibilities. Moreover, a firm support of association between chronic hepatitis and celiac disease remains largely unclear. Henceforth exploring cross-talk among these diseases will apparently lead to the promising discoveries concerning important genes and regulators
Methods: 321 and 1032 genes associated with celiac disease and hepatitis c retrieved from DisGeNET were subjected to build a gene regulatory network. Afterward a network-driven integrative analysis was performed to exploring prognosticates genes and related pathways
Results: 105 common genes between these diseases included 11 transcription factors were identified as hallmark molecules where by further screening enriched in biological GO terms and pathways chiefly in immune systems and signaling pathways such as chemokines, cytokines and interleukins
Conclusion: in silico data analysis approaches indicated that the identified selected combinations of genes covered a wide range of known functions triggering the inflammation implicated in these diseases
ABSTRACT
Aim: The main goal of this analysis was prioritization of co-expressed genes and miRNAs that are thought to have important influences in the pathogenesis of colon and lung cancers
Background: MicroRNAs [miRNAs] as small and endogenous noncoding RNAs which regulate gene expression by repressing mRNA translation or decreasing stability of mRNAs; they have proven pivotal roles in different types of cancers. Accumulating evidence indicates the role of miRNAs in a wide range of biological processes from oncogenesis and tumor suppressors to contribution to tumor progression. Colon and lung cancers are frequently encountered challenging types of cancers; therefore, exploring trade-off among underlying biological units such as miRNA with mRNAs will probably lead to identification of promising biomarkers involved in these malignancies
Methods: Colon cancer and lung cancer expression data were downloaded from Firehose and TCGA databases and varied genes extracted by DCGL software were subjected to build two gene regulatory networks by parmigene R package. Afterwards, a networkdriven integrative analysis was performed to explore prognosticates genes, miRNAs and underlying pathways
Results: A total of 192 differentially expressed miRNAs and their target genes within gene regulatory networks were derived by ARACNE algorithm. BTF3, TP53, MYC, CALR, NEM2, miR-29b-3p and miR-145 were identified as bottleneck nodes and enriched via biological gene ontology [GO] terms and pathways chiefly in biosynthesis and signaling pathways by further screening
Conclusion: Our study uncovered correlated alterations in gene expression that may relate with colon and lung cancers and highlighted the potent common biomarker candidates for the two diseases