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Abstract Carcinogenesis is a problem of global importance; since the incidence is increasing worldwide and therapeutic options are generally limited. Thus, it becomes imperative to find new therapeutic targets. In general, tumor growth is associated with both genetic and epigenetic aberrations resulting in altered gene expression. The acetylation and deacetylation of histones have been found to support to a substantial degree epigenetic regulation of gene expression. Histone deacetylase is a major player on gene expression leading to induction of chromatin relaxation and alteration of gene expression. So, its inhibition may selectively induce growth arrest, differentiation and apoptosis in tumor cells. Tumor cells are also exposed to several cell intrinsic and environmental perturbations that trigger a variety of adaptive mechanisms to favor cell transformation and promote cancer progression. In tumors, upregulation of unfolded protein response markers is often observed, indicating the occurrence of ER stress. Protein disulfide isomerase serves as a vital cellular defense against general protein misfolding via its chaperone activity. It is also responsible for the isomerization, formation and rearrangement of protein disulphide bonds, thereby providing another mechanism by which native protein. |