Introduction: Epigenetics and genetic alteration leads to cancer initiation and progression. Demethylation as an epigenetic factor that can contribute to cancer has already been known. Dnmts genes have been shown to play role in DNA methylation. Azacitidin as an inhibitor of Dnmts may lead to demethylation. Utilization of Azacitidin in vitro can help us modeling the mechanisms of diseases, especially cancer as a health issue. In this study we analyze data that gathered by RNA sequencing from the effect of usage of Azacitidin as a demethylation factor to elucidate the role of intracellular pathways that can play role in cancer pathogenesis.
Methods: With the assistance of bioinformatics we analysis ten files from NCBI and heat maps have been drawn. The significant subset of differentiated expressed genes have been extracted by GEO2R and network provided by string package.
Results: By analysis of this data, it has been shown that Azacitidin as a demethylation factor activates pathways in cancer such as p53 signaling that known as KEEG pathways. This data demonstrated that demethylation of Dnmt genes can leads to activation of pathways that closely related to cancer initiation and progression, as an epigenetic factor.
Conclusion: In the end, we can sum up that AZA-c which has been used by commercial name of Vidaza might initiate cancer successors which add its distractive effects to this supportive pathway to treat cancers. In here, we find that this substance have many additional benefits which take advantage of many other aspects in curing cancer cells.