DNA hypermethylation regulates the expression of members of the Mu-class glutathione S-transferases and glutathione peroxidases in Barrett's adenocarcinoma

Peng, Dunfa; Razvi, Mohammad; Chen, Heidi; Washington, Kay; Roessner, Albert; Schneider‐Stock, Regine; El–Rifai, Wael

doi:10.1136/gut.2007.146290

Cited by 165 publications

(170 citation statements)

References 47 publications

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“…However, increasing evidence suggests that GPx3 also possesses tumor suppressor activity (5,9,(22)(23)(24)(25)(26)(27)(28)(29). In this study, GPx3 carries out tumor suppressor signaling at least partly through the activation of PIG3, which is a protein associated with the generation of ROS that induces cell death.…”

Section: Discussionmentioning

confidence: 83%

p53-induced Gene 3 Mediates Cell Death Induced by Glutathione Peroxidase 3

Wang

Luo

Tan

et al. 2012

Journal of Biological Chemistry

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Background: Glutathione peroxidase 3 was identified as a new tumor suppressor. However, the mechanism is not clear. Results: Our analysis indicates that glutathione peroxidase 3 activates p53-induced gene 3 both in vivo and in vitro. Conclusion: p53-induced gene 3 is a major mediator of GPx3-induced cell death. Significance: Glutathione peroxidase 3-p53-induced gene 3 signaling represents a novel signaling pathway for cell death.

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Section: Discussionmentioning

confidence: 83%

p53-induced Gene 3 Mediates Cell Death Induced by Glutathione Peroxidase 3

Wang

Luo

Tan

et al. 2012

Journal of Biological Chemistry

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“…A significant overlap between the anti-Ikaros and anti-FLAG profiles of association was observed. Among the genes identified, we found several genes for which an association with colorectal adenocarcinoma had previously been reported, such as PTPN6 (25), which codes for protein tyrosine phosphatase, nonreceptor type; MEIS2 (26), a homeobox protein coding gene; and GPX7 (27), the glutathione peroxidase 7 gene.…”

Section: Identification Of Ikaros Direct Targets In Colorectal Cellsmentioning

confidence: 93%

Long-Range Epigenetic Silencing Associates with Deregulation of Ikaros Targets in Colorectal Cancer Cells

Javierre

Rodríguez-Ubreva

Al‐Shahrour

et al. 2011

Molecular Cancer Research

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Transcription factors are common targets of epigenetic inactivation in human cancer. Promoter hypermethylation and subsequent silencing of transcription factors can lead to further deregulation of their targets. In this study, we explored the potential epigenetic deregulation in cancer of Ikaros family genes, which code for essential transcription factors in cell differentiation and exhibit genetic defects in hematologic neoplasias. Unexpectedly, our analysis revealed that Ikaros undergoes very specific promoter hypermethylation in colorectal cancer, including in all the cell lines studied and around 64% of primary colorectal adenocarcinomas, with increasing proportions in advanced Duke's stages. Ikaros hypermethylation occurred in the context of a novel long-range epigenetic silencing (LRES) region. Reintroduction of Ikaros in colorectal cancer cells, ChIP-chip analysis, and validation in primary samples led us to identify a number of direct targets that are possibly related with colorectal cancer progression. Our results not only provide the first evidence that LRES can have functional specific effects in cancer but also identify several deregulated Ikaros targets that may contribute to progression in colorectal adenocarcinoma.

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“…As an example of a detailed study of one of the selected genes, GPX3 down-regulation due to promoter methylation is probably the first report in gastric cancer, following similar results in prostate cancer (21) and in Barrett's-related adenocarcinomas (32). We have shown through an immunohistostaining study of tissue microarrays that GPX3 is expressed at a significantly lower protein level in normal gastric tissues than in gastric cancer.…”

Section: Discussionmentioning

confidence: 82%

An 8-gene signature, including methylated and down-regulated glutathione peroxidase 3, of gastric cancer

Zhang

Yang²,

Kim³

et al. 2009

Int J Oncol

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Abstract.We have identified an 8-gene signature with significant expression differences between gastric cancer and normal gastric tissues. This 8-gene set can predict the normal and cancer status of gastric tissues with more than 96% accuracy in a totally independent microarray dataset. The 8 genes are composed of down-regulated KLF4, GPX3, SST and LIPF, together with up-regulated SERPINH1, THY1 and INHBA in gastric cancer. To corroborate the differential gene expression pattern, we chose GPX3 and examined its expression pattern in detail. A comparison of GPX3 expression pattern shows a broader down-regulated pattern in multiple types of cancers, including cervical, thyroid, head and neck, lung cancers and melanoma than in healthy controls. An immuno-histostaining analysis in tissue microarrays confirms GPX3 down-regulation in gastric cancer. Mechanism-wise GPX3 down-regulation in gastric cancer is due to promoter hypermethylation. Collectively, these results show a correct identification of 8 genes as gastric cancer biomarkers.

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DNA hypermethylation regulates the expression of members of the Mu-class glutathione S-transferases and glutathione peroxidases in Barrett's adenocarcinoma

Abstract: BACKGROUND-The accumulation of reactive oxygen species and subsequent oxidative DNA damage underlie the development of Barrett's esophagus (BE) and its progression to Barrett's dysplasia (BD) and adenocarcinoma (BAC).

Cited by 165 publications

References 47 publications

p53-induced Gene 3 Mediates Cell Death Induced by Glutathione Peroxidase 3

p53-induced Gene 3 Mediates Cell Death Induced by Glutathione Peroxidase 3

Long-Range Epigenetic Silencing Associates with Deregulation of Ikaros Targets in Colorectal Cancer Cells

An 8-gene signature, including methylated and down-regulated glutathione peroxidase 3, of gastric cancer

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