Document Type : Research Articles
Authors
1
Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
2
Department of Medical Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
3
Iranian Blood Transfusion Organization-Research Center, Iranian Blood Transfusion Organization, IBTO blg., Hemmat Exp. Way, Teheran, Iran.
4
Department of Medical Biotechnology, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
5
Department of Clinical Biochemistry and Laboratory Medicine, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Abstract
Colorectal cancer (CRC) is one of the most malignant cancers and results in a substantial rate of morbidity and mortality. Diagnosis of this malignancy in early stages increases the chance of effective treatment. High-throughput data analyses reveal omics signatures and also provide the possibility of developing computational models for early detection of this disease. Such models would be able to use as complementary tools for early detection of different types of cancers including CRC. In this study, using gene expression data, the Flux balance analysis (FBA) applied to decode metabolic fluxes in cancer and normal cells. Moreover, transcriptome and genome analyses revealed driver agents of CRC in a biological network scheme. By applying comprehensive publicly available data from TCGA, different aspect of CRC regulome including the regulatory effect of gene expression, methylation, microRNA, copy number aberration and point mutation profile over protein levels investigated and the results provide a regulatory picture underlying CRC. Compiling omics profiles indicated snapshots of changes in different omics levels and flux rate of CRC. In conclusion, considering obtained CRC signatures and their role in biological operating systems of cells, the results suggest reliable driver regulatory modules that could potentially serve as biomarkers and therapeutic targets and furthermore expand our understanding of driving mechanisms of this disease.
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