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  • br Conclusion The following is the supplementary data relate

    2019-07-08


    Conclusion The following is the supplementary data related to this article.
    Conflict of interest
    Substantial author contributions Andreina Bruno: to the conception and design of the study, to the acquisition, the interpretation and the analysis of data and to write the manuscript; Caterina Di Sano: to the analysis and the interpretation of the data; Francesco Lorusso: to the conception and design of the study and to the acquisition, the interpretation and the analysis of data; Paola Dino: to the analysis and the interpretation of the data; Domenica Russo: to the analysis and the interpretation of the data; Antonella Ballacchino: to the analysis and the interpretation of the data; Salvatore Gallina: to the conception and design of the study and to the interpretation of the data; Domenico Michele Modica: to the interpretation of the data; Giuseppina Chiappara: to the interpretation of the data; Hans-Uwe Simon: to the analysis and the interpretation of the data and to revise critically the paper for important intellectual content for final approval of the version to be submitted; Elisabetta Pace: to the analysis and the interpretation of the data and to revise critically the paper for important intellectual content for final approval of the version to be submitted.
    Transparency document
    Introduction Cancer is a heterogeneous group of disease associated with genetic alternations, oncogene activation and tumor suppressor genes silencing [1]. Recent evidences suggest that, abnormalities or aberrant regulation of epigenetic modifications contribute significantly in tumorigenesis [[2], [3], [4]]. Epigenetic modifications involving DNA methylation, histone modification and micro RNA mediated gene regulation affects cellular physiology and function of both normal and cancer Minocycline HCl [[5], [6], [7], [8]] Genome wide hypo- and regional (gene promoter specific) hyper-methylation of DNA (aberrant DNA methylation) is one of the most important epigenetic alternations observed in mammalian genome that contributes to the transcriptional silencing of tumor suppressor genes [9,10]. Particularly, the hypermethylation of -CpG-island(s) of gene promoter in association with histone deacetylations plays crucial roles in repression of tumor suppressor genes [11,12] and frequently observed in multiple types of cancer [3,13,14]. Reversible chemical modifications of the chromatin proteins like acetylation and methylation of histones are two important molecular signatures for dynamic regulation of gene function and in this scenario DNA methylation augurs histone deacetylation to precipitate inactive genes. Dysregulation of these modifications are involved with tumor development and cancer progression [15]. Along with DNA methylation and histone modifications, dysregulation of genes that encode the proteins for DNA and histone modifications [for examples, DNA methyltransferases (DNMTs) and Histone deacetylases (HDACs)] also play active roles in tumor development and cancer progression affecting cell survival, migration and invasion [16,17]. E-cadherin, a cell surface glycoprotein and member of cadherin family, plays important role in tissue integrity and reduces cell motility; hence, it is termed as tumor suppressor gene. E-cadherin also plays important roles in cellular migration, maintaining cell polarity and structure of normal epithelial cells [18]. Downregulation of E-cadherin is associated with enhanced epithelial to mesenchymal transition (EMT), aggressiveness, invasion and metastasis of breast cancer cells and well documented that CDH1 gene is inhibited by activation, nuclear translocation and binding of transcription factors such as Snail, Slug and Twist on the promoter of CDH1 [[19], [20], [21], [22], [23]]. We and other laboratories reported that, CDH1 gene silencing by promoter hypermethylation is the main cause of E-cadherin protein scarcity in breast cancer [[24], [25], [26]].