MGMT-B Gene Promoter Hypermethylation in Patients with Inflammatory Bowel Disease - A Novel Finding

Mokarram, Pooneh; Kavousipour, Soudabeh; Sarabi, Mostafa Moradi; Mehrabani, Golnoush; Fahmidehkar, Mohammad Ali; Shamsdin, Seyedeh Azra; Alipour, Abbas; Naini, Mahvash Alizade

doi:10.7314/apjcp.2015.16.5.1945

Cited by 14 publications

(8 citation statements)

References 61 publications

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“…PRICKLE1 , SOX11 , TGFBR3 , NKX2-3 ) [54, 56, 58, 59], immune pathways such as the Wnt/NF-κβ (e.g. PITX2 , RARB , ROR1 , FOXA2 ) [58, 60], IL-23 pathways (e.g. STAT3 , BCL3 , OSM , TLR4 ) [53, 61] and inflammation-associated genes (e.g.…”

Section: Dna Methylation Studies In As Ibd and Psoriasismentioning

confidence: 99%

Best practices in DNA methylation: lessons from inflammatory bowel disease, psoriasis and ankylosing spondylitis

et al. 2019

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Advances in genomic technology have enabled a greater understanding of the genetics of common immune-mediated diseases such as ankylosing spondylitis (AS), inflammatory bowel disease (IBD) and psoriasis. The substantial overlap in genetically identified pathogenic pathways has been demonstrated between these diseases. However, to date, gene discovery approaches have only mapped a minority of the heritability of these common diseases, and most disease-associated variants have been found to be non-coding, suggesting mechanisms of disease-association through transcriptional regulatory effects. Epigenetics is a major interface between genetic and environmental modifiers of disease and strongly influence transcription. DNA methylation is a well-characterised epigenetic mechanism, and a highly stable epigenetic marker, that is implicated in disease pathogenesis. DNA methylation is an under-investigated area in immune-mediated diseases, and many studies in the field are affected by experimental design limitations, related to study design, technical limitations of the methylation typing methods employed, and statistical issues. This has resulted in both sparsity of investigations into disease-related changes in DNA methylation, a paucity of robust findings, and difficulties comparing studies in the same disease. In this review, we cover the basics of DNA methylation establishment and control, and the methods used to examine it. We examine the current state of DNA methylation studies in AS, IBD and psoriasis; the limitations of previous studies; and the best practices for DNA methylation studies. The purpose of this review is to assist with proper experimental design and consistency of approach in future studies to enable a better understanding of the functional role of DNA methylation in immune-mediated disease.

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Section: Dna Methylation Studies In As Ibd and Psoriasismentioning

confidence: 99%

Best practices in DNA methylation: lessons from inflammatory bowel disease, psoriasis and ankylosing spondylitis

et al. 2019

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“…It has been established that epigenetic alteration machinery such as regional hypermethylation and global DNA hypomethylation, are accepted processes and hallmarks of cancer cells that may lead to modifications, including loss of imprinting, and are antecedents to the classical primary transforming events such as chromosomal instability, and mutations in tumor suppressors and proto-oncogenes[44]. Moreover, DNA hypermethylation of TSGs, involved in cell-cycle regulation, DNA repair, apoptosis, angiogenesis, adhesion, and invasion, is the most common change in tumorigenesis, causing gene silencing at the transcription level, and a failure of typical cellular functions[13,45-48]. On the other hand, DNA hypermethylation of CpG islands often affects transcriptional silencing of tumor suppressor or DNA repair genes, although there are exceptions[49-51].…”

Section: Dna Hypermethylation and Colorectal Cancermentioning

confidence: 99%

Polyunsaturated fatty acids and DNA methylation in colorectal cancer

Sarabi

Khorramabadi

Zare

et al. 2019

WJCC

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Colorectal cancer (CRC) has been designated a major global problem, especially due to its high prevalence in developed countries. CRC mostly occurs sporadically (75%-80%), and only 20%-25% of patients have a family history. Several processes are involved in the development of CRC such as a combination of genetic and epigenetic alterations. Epigenetic changes, including DNA methylation play a vital role in the progression of CRC. Complex interactions between susceptibility genes and environmental factors, such as a diet and sedentary lifestyle, lead to the development of CRC. Clinical and experimental studies have confirmed the beneficial effects of dietary polyunsaturated fatty acids (PUFAs) in preventing CRC. From a mechanistic viewpoint, it has been suggested that PUFAs are pleiotropic agents that alter chromatin remodeling, membrane structure and downstream cell signaling. Moreover, PUFAs can alter the epigenome via modulation of DNA methylation. In this review, we summarize recent investigations linking PUFAs and DNA methylation-associated CRC risk.

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“…There has also been extensive research on changes in DNA methylation to discover diagnostic biomarkers for IBD (10)(11)(12). Changes in DNA methylation in various gene pathways, including immune pathways (13,14), interleukins (15,16), Toll-Like Receptors (16), and in ammatory pathways (17,18), have been observed in IBD. However, to date, there is no standard database of methylated genes in IBD (10).…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the TLR 4 and TLR 5 genes methylation and mRNA expression in patients with Inflammatory Bowel Disease

Asadzadeh‐Aghdaei

Nourian

Chaleshi

et al. 2023

Preprint

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Background Immune system dysfunction, especially Toll-Like Receptors (TLRs), is a major factor in the pathogenesis of IBD. The functional roles of TLR4 and TLR5 as mediators of innate immune responses to pathogenic microbes in the gastrointestinal tract and their association with epigenetic alterations in the pathogenesis of this disease are very important. We aimed to investigate the aberrant methylation changes in TLR4 and TLR5 gene promoter DNA sequences and evaluate the association of TLR4 and TLR5 gene expression with IBD patient subtypes. Methods This case-control study was performed on the tissues of 33 patients with inflammatory bowel disease and 20 healthy controls. After RNA extraction and cDNA synthesis, the expression of TLR4 and TLR5 was examined using qRT-PCR. In addition, following DNA extraction and treatment with sodium bisulfite, the variation in the methylation rate of TLR4 and TLR5 gene promoters was evaluated using High Resolution Melting (HRM) method. Results According to the findings, TLR4 expression increased in the Ulcerative colitis patients compared to the control group (P = 0.0385) but the expression of TLR5 gene in the patients with Ulcerative colitis (UC) and Crohn disease (CD) did not change compared to the control group (P = 0.2710). In addition, no significant correlation was found between the expression of TLR4 and TLR5 and sex. In addition, a significant different was observed in the TLR4 promoter methylation pattern between, UC and normal tissues (P = 0.028), also, a significant different was observed in the TLR4 promoter methylation between, CD and normal tissues (P = 0.006), but in TLR5 this difference was not significant. Conclusion These data suggest that the increased expression of TLR4 and aberrant methylation changes indicate the importance of this gene in the pathogenesis of IBD and its role as a biomarker in IBD patients.

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MGMT-B Gene Promoter Hypermethylation in Patients with Inflammatory Bowel Disease - A Novel Finding

Cited by 14 publications

References 61 publications

Best practices in DNA methylation: lessons from inflammatory bowel disease, psoriasis and ankylosing spondylitis

Best practices in DNA methylation: lessons from inflammatory bowel disease, psoriasis and ankylosing spondylitis

Polyunsaturated fatty acids and DNA methylation in colorectal cancer

Evaluation of the TLR 4 and TLR 5 genes methylation and mRNA expression in patients with Inflammatory Bowel Disease

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