Folate deprivation enhances invasiveness of human colon cancer cells mediated by activation of sonic hedgehog signaling through promoter hypomethylation and cross action with transcription nuclear factor-kappa B pathway

Wang, Tz-Ping; Hsu, Shu‐Han; Feng, Hsin-Chun; Huang, Rachel

doi:10.1093/carcin/bgs138

Cited by 56 publications

(61 citation statements)

References 50 publications

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“…In stark contrast to hypermethylation, promoter hypomethylation can lead to increased expression of oncogenes (Igor and Frederick, 2009;Wang et al, 2012). Interestingly, only genes with hypomethylated loci outside the promoter region were found in our study.…”

Section: Discussioncontrasting

confidence: 45%

Genome-wide Analysis of Aberrant DNA Methylation for Identification of Potential Biomarkers in Colorectal Cancer Patients

Fang¹,

Zheng²,

Wu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background: Colorectal cancer is one of the leading causes of mortality worldwide. Genome wide analysis studies have identified sequence mutations causing loss-of-function that are associated with disease occurrence and severity. Epigenetic modifications, such DNA methylation, have also been implicated in many cancers but have yet to be examined in the East Asian population of colorectal cancer patients. Methods: Biopsies of tumors and matched non-cancerous tissue types were obtained and genomic DNA was isolated and subjected to the bisulphite conversion method for comparative DNA methylation analysis on the Illumina Infinium HumanMethylation27 BeadChip. Results: Totals of 258 and 74 genes were found to be hyper-and hypo-methylated as compared to the individual's matched control tissue. Interestingly, three genes that exhibited hypermethylation in their promoter regions, CMTM2, ECRG4, and SH3GL3, were shown to be significantly associated with colorectal cancer in previous studies. Using heatmap cluster analysis, eight hypermethylated and 10 hypomethylated genes were identified as significantly differentially methylated genes in the tumour tissues. Conclusions: Genome-wide methylation profiling facilitates rapid and simultaneous analysis of cancerous cells which may help to identify methylation markers with high sensitivity and specificity for diagnosis and prognosis. Our results show the promise of the microarray technology in identification of potential methylation biomarkers for colorectal cancers.

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Section: Discussioncontrasting

confidence: 45%

Genome-wide Analysis of Aberrant DNA Methylation for Identification of Potential Biomarkers in Colorectal Cancer Patients

Fang¹,

Zheng²,

Wu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…On the other hand, in vitro studies indicate that low levels of folic acid contribute to colon invasion by malignant cells [31].…”

Section: Fruits and Vegetablesmentioning

confidence: 99%

Diet and colorectal cancer

2015

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“…In this way, a recent study highlighted that, when compared with individuals placed on a normal diet, individuals fed a high lipid diet on a very short period exhibit a modification of the methylome of muscular cells affecting principally genes implicated in the inflammatory response, the reproductive system, and cancer (5). Another recent study also showed that a deprivation in folate led to an increase in the invasive character of human colic cancer cells through hypomethylation of the promoter region of the Sonic-hedgehog oncogene and activation of the NF-κB signaling pathway (6). Whereas these two studies among many others lend weight to the hypothesis of a close relationship between nutritional disorders, epigenetic reprograming, and cancer, the underlying mechanisms are still poorly understood.…”

Section: Introductionmentioning

confidence: 99%

O-GlcNAcylation, an Epigenetic Mark. Focus on the Histone Code, TET Family Proteins, and Polycomb Group Proteins

2014

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There are increasing evidences that dietary components and metabolic disorders affect gene expression through epigenetic mechanisms. These observations support the notion that epigenetic reprograming-linked nutrition is connected to the etiology of metabolic diseases and cancer. During the last 5 years, accumulating data revealed that the nutrient-sensing O-GlcNAc glycosylation (O-GlcNAcylation) may be pivotal in the modulation of chromatin remodeling and in the regulation of gene expression by being part of the “histone code,” and by identifying OGT (O-GlcNAc transferase) as an interacting partner of the TET family proteins of DNA hydroxylases and as a member of the polycomb group proteins. Thus, it is suggested that O-GlcNAcylation is a post-translational modification that links nutrition to epigenetic. This review summarizes recent findings about the interplay between O-GlcNAcylation and the epigenome and enlightens the contribution of the glycosylation to epigenetic reprograming.

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Folate deprivation enhances invasiveness of human colon cancer cells mediated by activation of sonic hedgehog signaling through promoter hypomethylation and cross action with transcription nuclear factor-kappa B pathway

Cited by 56 publications

References 50 publications

Genome-wide Analysis of Aberrant DNA Methylation for Identification of Potential Biomarkers in Colorectal Cancer Patients

Genome-wide Analysis of Aberrant DNA Methylation for Identification of Potential Biomarkers in Colorectal Cancer Patients

Diet and colorectal cancer

O-GlcNAcylation, an Epigenetic Mark. Focus on the Histone Code, TET Family Proteins, and Polycomb Group Proteins

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