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Review
. 2015:2015:201703.
doi: 10.1155/2015/201703. Epub 2015 Mar 1.

Epigenetic regulation of inflammatory cytokines and associated genes in human malignancies

Rehana Yasmin  1 , Sami Siraj  2 , Amjad Hassan  1 , Abdul Rehman Khan  1 , Rashda Abbasi  3 , Nafees Ahmad  3
Affiliations
Review

Epigenetic regulation of inflammatory cytokines and associated genes in human malignancies

Rehana Yasmin et al. Mediators Inflamm. 2015.

Abstract

Inflammation is a multifaceted defense response of immune system against infection. Chronic inflammation has been implicated as an imminent threat for major human malignancies and is directly linked to various steps involved in tumorigenesis. Inflammatory cytokines, interleukins, interferons, transforming growth factors, chemokines, and adhesion molecules have been associated with chronic inflammation. Numerous cytokines are reported to be aberrantly regulated by different epigenetic mechanisms like DNA methylation and histone modifications in tumor tissues, contributing to pathogenesis of tumor in multiple ways. Some of these cytokines also work as epigenetic regulators of other crucial genes in tumor biology, either directly or indirectly. Such regulations are reported in lung, breast, cervical, gastric, colorectal, pancreatic, prostate, and head and neck cancers. Epigenetics of inflammatory mediators in cancer is currently subject of extensive research. These investigations may help in understanding cancer biology and to develop effective therapeutic strategies. The purpose of this paper is to have a brief view of the aberrant regulation of inflammatory cytokines in human malignancies.

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Figures

Figure 1
Figure 1
Overview of different epigenetic mechanisms involved in the regulation of chromatin (heterochromatin and euchromatin). Histone acetylation catalyzed by histone acetylase (HAT) that slightly unwraps the DNA from histones and promotes gene expression. Histone deacetylation is catalyzed by histone deacetylase (HADC), which tightens the DNA and histone core together and represses transcription. CpG islands are mostly located in the regulatory regions of genome. DNA methyltransferase (DNMT) adds methyl group to the CpG site, which is the main epigenetic mechanism reported for transcriptional repression.
Figure 2
Figure 2
A schematic presentation elaborating epigenetic regulation of CD133 by TGF-β1 mediated by DNA methyltransferase (DNMT-1) in Huh 7 cell (HCC cell line). (a) Low expression of TGF-β1 does not affect DNMT-1 and thus methylation of CD133 promoter is maintained. (b) Elevated expression of TGF-β1 inhibits DNMT-1 which results in demethylation of CD133 promoter resulting in the initiation of transcription.
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