<i>MUC1</i> Expression Is Regulated by DNA Methylation and Histone H3 Lysine 9 Modification in Cancer Cells

Yamada, Norishige; Nishida, Yukari; Tsutsumida, Hideaki; Hamada, Tomofumi; Goto, Masamichi; Higashi, Michiyo; Nomoto, Mitsuharu; Yonezawa, Suguru

doi:10.1158/0008-5472.can-07-6844

Cited by 103 publications

(112 citation statements)

References 31 publications

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“…A previous work has shown that MUC1, a membrane bound mucin expressed on the surface of gastric epithelial cells, provides a protective barrier against H.pylori infection. MUC1 gene expression is regulated by DNA methylation, for instance, MUC1 mRNA expression in MUC1-negative cells was restored by the treatment with (Yamada et al, 2008). The luciferase assay demonstrated that the promoter activity of rs1550117 A allele of DNMT3a was significantly higher (more than two fold) than the G allele in Fan's study (Fan et al, 2010).…”

Section: Discussionmentioning

confidence: 96%

DNMT3a rs1550117 Polymorphism Association with Increased Risk of Helicobacter pylori Infection

Cao

Jia²,

Cao³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 96%

DNMT3a rs1550117 Polymorphism Association with Increased Risk of Helicobacter pylori Infection

Cao

Jia²,

Cao³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Quantitative methylation analysis of the MUC4 promoter was performed using the MassARRAY compact system (Hitachi high technologies corporation, Tokyo, Japan; Ehrich et al, 2005;Yamada et al, 2008). DNA from the cell lines was extracted using a DNeasy tissue system (Qiagen).…”

Section: Quantitative Methylation Analysismentioning

confidence: 99%

“…We recently described the epigenetic regulation of the MUC1 gene (Yamada et al, 2008). Similarly to MUC1, MUC4 is a factor associated with poor prognosis in several carcinomas (Shibahara et al, 2004;Saitou et al, 2005;Tamada et al, 2006;Tsutsumida et al, 2007), and thus we hypothesised that MUC4 is also regulated by an epigenetic mechanism.…”

mentioning

confidence: 95%

Promoter CpG methylation in cancer cells contributes to the regulation of MUC4

et al. 2009

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Mucin 4 (MUC4) is a high molecular weight transmembrane mucin that is overexpressed in many carcinomas and is a risk factor associated with a poor prognosis. In this study, we show that the DNA methylation pattern is intimately correlated with MUC4 expression in breast, lung, pancreas and colon cancer cell lines. We mapped the DNA methylation status of 94 CpG sites from À3622 to þ 29 using MassARRAY analysis that utilises base-specific cleavage of nucleic acids. MUC4-negative cancer cell lines and those with low MUC4 expression (eg, A427) were highly methylated near the transcriptional start site, whereas MUC4-positive cell lines (eg, NCI-H292) had low methylation levels. Moreover, 5-aza-2 0 -deoxycytidine and trichostatin A treatment of MUC4-negative cells or those with low MUC4 expression caused elevation of MUC4 mRNA. Our results suggest that DNA methylation in the 5 0 flanking region play an important role in MUC4 gene expression in carcinomas of various organs. An understanding of epigenetic changes in MUC4 may contribute to the diagnosis of carcinogenic risk and prediction of outcome in patients with cancer.

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“…Both the long reaction time and the labor of this modification make this process hard. Thus, we used kit for modification and there are many studies which use these modification kits for their studies (16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

Promoter hypermethylation of p16 and APC in gastrointestinal cancer patients

Erdem¹,

Küçükyıldırım²,

Saglar³

et al. 2014

Turk J Gastroenterol

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Background/Aims: Cancer is a consequence of the disruption of cellular regulation. Epigenetic is one of the reasons of this disruption. Epigenetic factors play a role in the carcinogenesis by affecting proto-oncogenes and tumor suppressor genes and it is one of the most popular research areas in recent years. DNA methylation, which is an epigenetic mechanism, occurs in the early stages of tumorigenesis. Promoter methylation which causes the silence of tumor suppressor genes have been studied extensively in various tumor types. The aim of this study was to investigate promoter methylation of certain tumor suppressor genes, Cyclin-dependent kinase inhibitor 2A (p16) and Adenomatous polyposis coli (APC), which take part in gastrointestinal tumorigenesis. Materials and Methods: To detect the promoter methylation of p16 and APC genes, tissue samples from 20 gastrointestinal cancer patients and peripheral blood samples from 15 healthy individuals were collected for Methylation-Specific Polymerase Chain Reaction (MSP) analysis. Results: According to the statistical analysis, in tumor tissue, positive methylation ratio of p16 and APC genes was found respectively 30% (6/20) and 50% (10/20). The difference of promoter methylation of these genes between tumor tissues and control group was significantly observed (p=0.02 and 0.001, respectively). An alteration of promoter methylation of APC gene according to tumor localization was found (p=0.007), but there was no significant difference observed in p16. Conclusion: In our study, promoter methylation which was considered to be occurred as an early event in gastrointestinal carcinogenesis was observed in p16 and APC genes.

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MUC1 Expression Is Regulated by DNA Methylation and Histone H3 Lysine 9 Modification in Cancer Cells

Cited by 103 publications

References 31 publications

DNMT3a rs1550117 Polymorphism Association with Increased Risk of Helicobacter pylori Infection

DNMT3a rs1550117 Polymorphism Association with Increased Risk of Helicobacter pylori Infection

Promoter CpG methylation in cancer cells contributes to the regulation of MUC4

Promoter hypermethylation of p16 and APC in gastrointestinal cancer patients

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