Methylation of NF-κB and its Role in Gene Regulation

Wang, Han; Prabhu, Lakshmi; Hartley, Antja-Voy; Martin, Matthew; Sun, Emily; Jiang, Guanglong; Liu, Yunlong; Lü, Tao

doi:10.5772/intechopen.72552

Cited by 7 publications

(4 citation statements)

References 45 publications

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“…In agreement with DNA methylation modification, HG exposure induced a TET2 upregulation and an increase of NF‐κB and NFKB target gene expression. Although, our “in vitro” experimental approach is not specific enough to address a direct causal link between DNA demethylation and gene expression, previous studies already demonstrated that NF‐κB promoter activity is regulated by its methylation levels 31 . Indeed, the observed decrease in SOD2 mRNA expression suggest that SOD2 promoter methylation, of the analyzed CpG positions, is not causally linked with SOD2 mRNA expression levels.…”

Section: Discussionmentioning

confidence: 93%

Incretin drugs effect on epigenetic machinery: New potential therapeutic implications in preventing vascular diabetic complications

et al. 2020

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The effect of GLP-1R agonists on DNA methylation levels of NF-κB and SOD2 genes in human aortic endothelial cells exposed to high glucose and in diabetic patients treated and not with incretin-based drugs, was evaluated. Methylation levels, mRNA and protein expression of NF-κB and SOD2 genes were measured in human endothelial cells exposed to high glucose for 7 days and treated with GLP-1R agonists. Methylation status of NF-κB and SOD2 promoter was also analyzed in 128 diabetics and 116 nondiabetics and correlated with intima media thickness (ITM), an early marker of atherosclerotic process. Cells exposed to high glucose showed lower NF-κB and SOD2 methylation levels, increased NF-κB and reduced SOD2 expression compared to normal glucose cells. Co-treatment with GLP-1 agonists prevented methylation and genes expression changes induced by high glucose. Both high glucose and incretins exposure increased DNA methyltransferases and demethylases levels. In diabetics, incretin treatment resulted a significant predictor of NF-κB DNA methylation, independently of age, sex, body mass index (BMI), glucose and plasma lipid levels. NF-κB DNA methylation inversely correlated with IMT after adjusting for multiple covariates. Our results firstly provide new evidences of an additional mechanism by which incretin drugs could prevent vascular diabetic complications. K E Y W O R D S atherosclerosis progression, DNA methylation, incretin based drugs, type 2 diabetes 2 | SCISCIOLA et AL.

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Section: Discussionmentioning

confidence: 93%

Incretin drugs effect on epigenetic machinery: New potential therapeutic implications in preventing vascular diabetic complications

et al. 2020

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“…NF-κB Signaling NF-κB comprises a family of five transcription factors that regulate the expression of a variety of genes involved in several biological processes. These processes include inflammation, cellular development and differentiation, cell cycle progression, cell migration and so on [43]. The members of the NF-κB family include RelA/p65, RelB, c-Rel, NF-κB1(p50/p105) and NF-κB2(p52/p100), and they function as dimers in two separate but interconnected arms of the NF-κB pathway: the canonical pathway and the non-canonical pathway.…”

Section: Nf-κb Signaling and Its Important Role In Crcmentioning

confidence: 99%

The Pivotal Player: Components of NF-κB Pathway as Promising Biomarkers in Colorectal Cancer

Martin

Sun

Motolani

et al. 2021

IJMS

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Over the last several decades, colorectal cancer (CRC) has been one of the most prevalent cancers. While significant progress has been made in both diagnostic screening and therapeutic approaches, a large knowledge gap still remains regarding the early identification and treatment of CRC. Specifically, identification of CRC biomarkers that can help with the creation of targeted therapies as well as increasing the ability for clinicians to predict the biological response of a patient to therapeutics, is of particular importance. This review provides an overview of CRC and its progression stages, as well as the basic types of CRC biomarkers. We then lay out the synopsis of signaling pathways related to CRC, and further highlight the pivotal and multifaceted role of nuclear factor (NF) κB signaling in CRC. Particularly, we bring forth knowledge regarding the tumor microenvironment (TME) in CRC, and its complex interaction with cancer cells. We also provide examples of NF-κB signaling-related CRC biomarkers, and ongoing efforts made at targeting NF-κB signaling in CRC treatment. We conclude and anticipate that with more emerging novel regulators of the NF-κB pathway being discovered, together with their in-depth characterization and the integration of large groups of genomic, transcriptomic and proteomic data, the day of successful development of more ideal NF-κB inhibitors is fast approaching.

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“…NF-κB dimer consists of p50 subunit and RELA /c-REL are bound to IκB proteins, whereas subunits of p50/RELA/c-REL are associated with p105. Eventually, activated dimers translocate to the nucleus, where induce transcription of NF-κB target genes [15][16][17]. Non-canonical NF-κB activation is slow and long-lasting and occurs upon stimulation of a certain TNFRs superfamily members such as B cell activating factor receptor (BAFFR), CD40, receptor activator of NF-κB (RANK), lymphotoxin-β receptor (LT-βR) [18,19].…”

Section: Nf-κb Signaling Pathway and Tumorigenesismentioning

confidence: 99%

The interplay between EBV and KSHV viral products and NF-κB pathway in oncogenesis

Charostad

Nakhaie

Dehghani

et al. 2020

Infect Agents Cancer

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Among the DNA tumor viruses Epstein-Barr virus (EBV) and Kaposi sarcoma herpesvirus (KSHV), account for a considerable percentage of virus-associated cancers. Deregulation of transcription factors signaling pathways is one of the most significant oncogenic characteristics of EBV and KSHV. NF-κB is a transcription factor that play a remarkable role in oncogenesis because of its function as a master regulator of a spectrum of genes involved in physiological and pathophysiological process. Constitutive activation of NF-κB is a frequent and well-described event in many human malignancies. Compelling evidence represent EBV and KSHV are capable of targeting different components of NF-κB cascade. Here, we summarized recent findings to clarify the precise relationship between dysregulation of NF-κB and EBV and KSHV-related malignancies. This essay also emphasizes on contribution of various viral products in developing cancer through alteration of NF-κB signaling pathway.

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Methylation of NF-κB and its Role in Gene Regulation

Cited by 7 publications

References 45 publications

Incretin drugs effect on epigenetic machinery: New potential therapeutic implications in preventing vascular diabetic complications

Incretin drugs effect on epigenetic machinery: New potential therapeutic implications in preventing vascular diabetic complications

The Pivotal Player: Components of NF-κB Pathway as Promising Biomarkers in Colorectal Cancer

The interplay between EBV and KSHV viral products and NF-κB pathway in oncogenesis

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