Crosstalk Between Inflammatory Signaling and Methylation in Cancer

Inflammation is an intricate immune response against infection and tissue damage. While the initial immune response is important for preventing tumorigenesis, chronic inflammation is implicated in cancer pathogenesis. It has been linked to various stages of tumor development including transformation...

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Autores principales:	Dipanwita Das, Nandini Karthik, Reshma Taneja
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	cancer inflammation epigenetics DNA methylation histone methylation 2 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/01d57720e9714d39881f915e344cf269
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spelling	oai:doaj.org-article:01d57720e9714d39881f915e344cf2692021-11-30T19:01:33ZCrosstalk Between Inflammatory Signaling and Methylation in Cancer2296-634X10.3389/fcell.2021.756458https://doaj.org/article/01d57720e9714d39881f915e344cf2692021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcell.2021.756458/fullhttps://doaj.org/toc/2296-634XInflammation is an intricate immune response against infection and tissue damage. While the initial immune response is important for preventing tumorigenesis, chronic inflammation is implicated in cancer pathogenesis. It has been linked to various stages of tumor development including transformation, proliferation, angiogenesis, and metastasis. Immune cells, through the production of inflammatory mediators such as cytokines, chemokines, transforming growth factors, and adhesion molecules contribute to the survival, growth, and progression of the tumor in its microenvironment. The aberrant expression and secretion of pro-inflammatory and growth factors by the tumor cells result in the recruitment of immune cells, thus creating a mutual crosstalk. The reciprocal signaling between the tumor cells and the immune cells creates and maintains a successful tumor niche. Many inflammatory factors are regulated by epigenetic mechanisms including DNA methylation and histone modifications. In particular, DNA and histone methylation are crucial forms of transcriptional regulation and aberrant methylation has been associated with deregulated gene expression in oncogenesis. Such deregulations have been reported in both solid tumors and hematological malignancies. With technological advancements to study genome-wide epigenetic landscapes, it is now possible to identify molecular mechanisms underlying altered inflammatory profiles in cancer. In this review, we discuss the role of DNA and histone methylation in regulation of inflammatory pathways in human cancers and review the merits and challenges of targeting inflammatory mediators as well as epigenetic regulators in cancer.Dipanwita DasNandini KarthikReshma TanejaFrontiers Media S.A.articlecancerinflammationepigeneticsDNA methylationhistone methylation 2Biology (General)QH301-705.5ENFrontiers in Cell and Developmental Biology, Vol 9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	cancer inflammation epigenetics DNA methylation histone methylation 2 Biology (General) QH301-705.5
spellingShingle	cancer inflammation epigenetics DNA methylation histone methylation 2 Biology (General) QH301-705.5 Dipanwita Das Nandini Karthik Reshma Taneja Crosstalk Between Inflammatory Signaling and Methylation in Cancer
description	Inflammation is an intricate immune response against infection and tissue damage. While the initial immune response is important for preventing tumorigenesis, chronic inflammation is implicated in cancer pathogenesis. It has been linked to various stages of tumor development including transformation, proliferation, angiogenesis, and metastasis. Immune cells, through the production of inflammatory mediators such as cytokines, chemokines, transforming growth factors, and adhesion molecules contribute to the survival, growth, and progression of the tumor in its microenvironment. The aberrant expression and secretion of pro-inflammatory and growth factors by the tumor cells result in the recruitment of immune cells, thus creating a mutual crosstalk. The reciprocal signaling between the tumor cells and the immune cells creates and maintains a successful tumor niche. Many inflammatory factors are regulated by epigenetic mechanisms including DNA methylation and histone modifications. In particular, DNA and histone methylation are crucial forms of transcriptional regulation and aberrant methylation has been associated with deregulated gene expression in oncogenesis. Such deregulations have been reported in both solid tumors and hematological malignancies. With technological advancements to study genome-wide epigenetic landscapes, it is now possible to identify molecular mechanisms underlying altered inflammatory profiles in cancer. In this review, we discuss the role of DNA and histone methylation in regulation of inflammatory pathways in human cancers and review the merits and challenges of targeting inflammatory mediators as well as epigenetic regulators in cancer.
format	article
author	Dipanwita Das Nandini Karthik Reshma Taneja
author_facet	Dipanwita Das Nandini Karthik Reshma Taneja
author_sort	Dipanwita Das
title	Crosstalk Between Inflammatory Signaling and Methylation in Cancer
title_short	Crosstalk Between Inflammatory Signaling and Methylation in Cancer
title_full	Crosstalk Between Inflammatory Signaling and Methylation in Cancer
title_fullStr	Crosstalk Between Inflammatory Signaling and Methylation in Cancer
title_full_unstemmed	Crosstalk Between Inflammatory Signaling and Methylation in Cancer
title_sort	crosstalk between inflammatory signaling and methylation in cancer
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/01d57720e9714d39881f915e344cf269
work_keys_str_mv	AT dipanwitadas crosstalkbetweeninflammatorysignalingandmethylationincancer AT nandinikarthik crosstalkbetweeninflammatorysignalingandmethylationincancer AT reshmataneja crosstalkbetweeninflammatorysignalingandmethylationincancer
_version_	1718406301654974464

Crosstalk Between Inflammatory Signaling and Methylation in Cancer

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