Epigenetic alterations of <i>CYLD</i> promoter modulate its expression in gastric adenocarcinoma: A footprint of infections

Ghadami, Elham; Nikbakhsh, Novin; Fattahi, Sadegh; Kosari-Monfared, Mohadeseh; Ranaee, Mohammad; Taheri, Hassan; Amjadi‐Moheb, Fatemeh; Godazandeh, Gholamali; Shafaei, Shahryar; Nosrati, Anahita; Langroudi, Maryam Pilehchian; Samadani, Ali Akbar; Amirbozorgi, Galia; Mirnia, Vahideh; Akhavan‐Niaki, Haleh

doi:10.1002/jcp.27220

Cited by 30 publications

(16 citation statements)

References 50 publications

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“…Deregulation of CYLD , a tumor suppressor gene, has been found in different types of cancer. Association between H. pylori infections with hypermethylation and reduced CYLD expression was observed in 10 out of 21 CagA-positive, H. pylori -infected tumor samples [60]. PTEN is another tumor suppressor gene, which serve important functions in apoptosis, cell cycle progression and cell proliferation.…”

Section: Genes Regulated By H Pylori-induced Dna Methylationmentioning

confidence: 99%

Helicobacter pylori-induced DNA Methylation as an Epigenetic Modulator of Gastric Cancer: Recent Outcomes and Future Direction

2019

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Gastric cancer is ranked fifth in cancer list and has the third highest mortality rate. Helicobacter pylori is a class I carcinogen and a predominant etiological factor of gastric cancer. H. pylori infection may induce carcinogenesis via epigenetic alterations in the promoter region of various genes. H. pylori is known to induce hypermethylation-silencing of several tumor suppressor genes in H. pylori-infected cancerous and H. pylori-infected non-cancerous gastric mucosae. This article presents a review of the published literature mainly from the last year 15 years. The topic focuses on H. pylori-induced DNA methylation linked to gastric cancer development. The authors have used MeSH terms “Helicobacter pylori” with “epigenetic,” “DNA methylation,” in combination with “gastric inflammation”, gastritis” and “gastric cancer” to search SCOPUS, PubMed, Ovid, and Web of Science databases. The success of epigenetic drugs such as de-methylating agents in the treatment of certain cancers has led towards new prospects that similar approaches could also be applied against gastric cancer. However, it is very important to understand the role of all the genes that have already been linked to H. pylori-induced DNA methylation in order to in order to evaluate the potential benefits of epigenetic drugs.

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Section: Genes Regulated By H Pylori-induced Dna Methylationmentioning

confidence: 99%

Helicobacter pylori-induced DNA Methylation as an Epigenetic Modulator of Gastric Cancer: Recent Outcomes and Future Direction

2019

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“…Epigenetics consist of DNA methylation, histone modification, histone acetylation, histone phosphorylation and also RNA remodeling which DNA methylation is the most important element [6][7][8][9][10][11][12]. Meanwhile, alongside with the investigation of epigenetics fluctuation in GI cancers, gene expression study must be added in order to have a better comparison and result [13][14][15][16][17][18][19][20].…”

Section: Epigenetic and Cancermentioning

confidence: 99%

Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer

Babaei¹,

Khaksar²,

Zeinali³

et al. 2019

BioMedicine

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Colorectal cancer (CRC) is distinguished by epigenetic elements like DNA methylation, histone modification, histone acetylation and RNA remodeling which is related with genomic instability and tumor initiation. Correspondingly, as a main epigenetic regulation, DNA methylation has an impressive ability in order to be used in CRC targeted therapy. Meaningly, DNA methylation is identified as one of most important epigenetic regulators in gene expression and is considered as a notable potential driver in tumorigenesis and carcinogenesis through gene-silencing of tumor suppressors genes. Abnormal methylation situation, even in the level of promoter regions, does not essentially change the gene expression levels, particularly if the gene was become silenced, leaving the mechanisms of methylation without any response. According to the methylation situation which has a strong eagerness to be highly altered on CpG islands in carcinogenesis and tumorigenesis, considering its epigenetic fluctuations in finding new biomarkers is of great importance. Modifications in DNA methylation pattern and also enrichment of methylated histone signs in the promoter regions of some certain genes like MUTYH, KLF4/6 and WNT1 in different signaling pathways could be a notable key contributors to the upregulation of tumor initiation in CRC. These epigenetic alterations could be employed as a practical diagnostic biomarkers for colorectal cancer. In this review, we will be discuss these fluctuations of MUTYH, KLF4/6 and WNT1 genes in CRC.

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“…By the way, the quality and quantity of extracted nucleic acids including DNA and RNA alongside compatible primers are of great importance. [30][31][32][33]…”

Section: Discussionmentioning

confidence: 99%

The fluctuation of APC gene in WNT signaling with adenine deletion of adenomatous polyposis coli, is associated in colorectal cancer

Norollahi

Hamidian

Kohpar

et al. 2020

Journal of Coloproctology

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Colorectal cancer is one of the most important malignancies in the classification of gastrointestinal cancers. One of the predisposing factors at molecular level for this cancer is via WNT signaling which is associated with the vast numbers of different genes. Thus, in this study, we aimed to investigate whether Adenomatous Polyposis Coli gene (APC) mutation of rs41115in two locations such as 132.002 and 131.989 acts as a trigger or cause of colorectal cancer. Relatively, 30 blood samples of colorectal cancer patients and 30 normal blood samples as control group after colonoscopy and also confirmation of pathology report at Rohani Hospital in Babol (Iran) were investigated. The primers were designed in order to be included the rs41115 to identify the particular polymorphisms of gene. The polymerase chain reaction (PCR direct sequencing method) was used. Conclusively, deletion of adenine in two specific locations such as 131.989 and 132.002 has been identified, but there was no relationship between rs41115 polymorphisms located in adenomatous polyposis coli gene and colorectal cancer.

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Epigenetic alterations of CYLD promoter modulate its expression in gastric adenocarcinoma: A footprint of infections

Cited by 30 publications

References 50 publications

Helicobacter pylori-induced DNA Methylation as an Epigenetic Modulator of Gastric Cancer: Recent Outcomes and Future Direction

Helicobacter pylori-induced DNA Methylation as an Epigenetic Modulator of Gastric Cancer: Recent Outcomes and Future Direction

Epigenetic profiling of MUTYH, KLF6, WNT1 and KLF4 genes in carcinogenesis and tumorigenesis of colorectal cancer

The fluctuation of APC gene in WNT signaling with adenine deletion of adenomatous polyposis coli, is associated in colorectal cancer

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