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Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (miRNA dataset)

ABSTRACT: Aberrant DNA methylation is frequently observed in cancer. The aim of this study was to determine how DNA methylation is changed after arsenic-induced malignant transformation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE38929 | GEO | 2012/06/26

SECONDARY ACCESSION(S): PRJNA169418

REPOSITORIES: GEO

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Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (miRNA dataset)

Project description:Aberrant DNA methylation is frequently observed in cancer. The aim of this study was to determine how DNA methylation is changed after arsenic-induced malignant transformation. Arsenite-transformed RWPE-1 cells (n=2) are compared to parental RWPE-1 cells (n=2). Normal PrEC (n=2) are included for comparison. Immunoprecipitation using anti-methylcytosine (5MeC) antibody.

2012-06-25 | E-GEOD-38929 | biostudies-arrayexpress

Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (MeDIP-chip dataset 2)

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Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (MeDIP-chip dataset 1)

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Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (MeDIP-chip dataset 1)

Project description:Aberrant DNA methylation is frequently observed in cancer. The aim of this study was to determine how DNA methylation is changed after toxicant-induced malignant transformation. This study also puts the DNA methylation changes into context with respect to the aberrant DNA methylation events that occur in bladder and prostate carcinogenesis not associated with toxicant exposure. Immortalized UROtsa (n=3) and RWPE-1 (n=2) are compared to normal HUC (n=2) and PrEC (n=2), respectively. Arsenite (n=1), monomethylarsonous acid (n=2) or cadmium (n=1) transformed UROtsa are compared to parental UROtsa (n=3). Arsenite (n=2), cadmium (n=1) or MNU (n=1) transformed RWPE-1 cells are compared to parental RWPE-1 cells (n=2). Clinical bladder tumor biopsies (n=6), urothelial carcinoma cell lines (n=2) and prostate cancer cell lines (n=3) are compared to thier normal tissue counterparts HUC (n=2) and PrEC (n=2). Immunoprecipitation using anti-methylcytosine (5MeC) antibody.

2012-06-25 | E-GEOD-38926 | biostudies-arrayexpress

Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (MeDIP-chip dataset 2)

2012-06-25 | E-GEOD-38928 | biostudies-arrayexpress

Patterns of aberrant DNA methylation after toxicant-induced malignant transformation

Project description:This SuperSeries is composed of the following subset Series: GSE38926: Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (MeDIP-chip dataset 1) GSE38928: Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (MeDIP-chip dataset 2) GSE38929: Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (miRNA dataset) Refer to individual Series

2012-06-25 | E-GEOD-38930 | biostudies-arrayexpress

Patterns of aberrant DNA methylation after toxicant-induced malignant transformation

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-06-26 | GSE38930 | GEO

Agglomerates of aberrant DNA methylation are associated with toxicant-induced malignant transformation.

Project description:Epigenetic dysfunction is a known contributor in carcinogenesis, and is emerging as a mechanism involved in toxicant-induced malignant transformation for environmental carcinogens such as arsenicals or cadmium. In addition to aberrant DNA methylation of single genes, another manifestation of epigenetic dysfunction in cancer is agglomerative DNA methylation, which can participate in long-range epigenetic silencing that targets many neighboring genes and has been shown to occur in several types of clinical cancers. Using in vitro model systems of toxicant-induced malignant transformation, we found hundreds of aberrant DNA methylation events that emerge during malignant transformation, some of which occur in an agglomerative fashion. In an arsenite-transformed prostate epithelial cell line, the protocadherin (PCDH), HOXC and HOXD gene family clusters are targeted for agglomerative DNA methylation. The agglomerative DNA methylation changes induced by arsenicals appear to be common and clinically relevant events, since they occur in other human cancer cell lines and models of malignant transformation, as well as clinical cancer specimens. Aberrant DNA methylation in general occurred more often within histone H3 lysine-27 trimethylation stem cell domains. We found a striking association between enrichment of histone H3 lysine-9 trimethylation stem cell domains and toxicant-induced agglomerative DNA methylation, suggesting these epigenetic modifications may become aberrantly linked during malignant transformation. In summary, we found an association between toxicant-induced malignant transformation and agglomerative DNA methylation, which lends further support to the hypothesis that epigenetic dysfunction plays an important role in toxicant-induced malignant transformation.

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The aberrant landscape of DNA methylation and gene expression during arsenic-induced cell transformation

Project description:We describe the alterations in DNA methylation around the promoter region and the impact on gene expression in HaCaT cells during the transformation process caused by chronic exposure to arsenic. Nucleic acids were extracted at the beginning of treatment and at weeks 0, 5, 15, and 25. Cell cultures with the same passage (week 25) and no arsenic treatment served as controls.

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The aberrant landscape of DNA methylation and gene expression during arsenic-induced cell transformation

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