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Reduction of DNA methylation suppresses colon carcinogenesis through induction of tumor cell differentiation

ABSTRACT: In this study, we analyzed global gene expressions of colon tumors from DNA hypomethylated and the control mice. We found that DNA hypomethylated tumors express significantly higher levels of intestinal differentiation-related genes when compared with the control tumors. These results suggest that DNA methylation may play a role in the maintenance of undifferentiated state of colon tumor cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE60620 | GEO | 2015/08/05

SECONDARY ACCESSION(S): PRJNA258660

REPOSITORIES: GEO

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Reduction of DNA methylation suppresses colon carcinogenesis through induction of tumor cell differentiation

Project description:In this study, we analyzed global gene expressions of colon tumors from DNA hypomethylated and the control mice. We found that DNA hypomethylated tumors express significantly higher levels of intestinal differentiation-related genes when compared with the control tumors. These results suggest that DNA methylation may play a role in the maintenance of undifferentiated state of colon tumor cells. Two different Dnmt1 mutant alleles were used in this study; hypomorphic Dnmt1chip allele and conventional KO Dnmt1c allele, which described previously. Previous studies indicated that Dnmt1chip/c mice have reduced DNA methylation contents at pericentromeric satellite repeats, while Dnmt1chip/+ mice have the same levels of genomic methylation as wildtype mice. Experimental mice in an isogenic F1 hybrid background were obtained by breeding Dnmt1c/+; ApcMin/+ mouse in the C57BL/6 background with Dnmt1chip/chip; Apc+/+ mouse in the 129Sv4 background. Six-week-old DNA hypomethylated (Dnmt1chip/c; ApcMin/+) and the control (Dnmt1chip/+; ApcMin/+) mice were fed with 2% (w/v) dextran sodium sulfate (DSS), a potent promoter for colon carcinogenesis. At 20 weeks of age, colon tumors were harvested from both cohorts (n=3 for both DNA hypomethylated tumors and the control tumors) and analyzed for their gene expressions.

2015-08-05 | E-GEOD-60620 | biostudies-arrayexpress

Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [RRBS]

Project description:We report a reprogrammable mouse system in which reprogramming factor expression in vivo can be controlled temporally by treatment with doxycycline (Dox). Transient expression of reprogramming factors in vivo results in tumor development in various tissues, consisting of undifferentiated dysplastic cells. We analyzed the kidney tumors developed in reprogrammable mice for global gene expressions and DNA methylations. Reprogrammable mice at 4 weeks of age were treated with Dox for 7 days followed by the withdrawal. Seven days after the withdrawal, kidney tumors were analyzed for gene expressions and DNA methylations with microarray and RRBS method, respectively. Normal kidney tissue at the same age and ES cells were analyzed as controls. To examine the early changes of gene expressions, transgene-expressing kidney cells were FACS sorted and they are utilized for microarray analysis. Primary liver tumors in reprogrammable mice and transplanted secondary kidney tumors in the subcutaneous tissues of immnodeficient mice were also analyzed for gene expressions.

2014-02-13 | E-GEOD-52303 | biostudies-arrayexpress

Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [array]

2014-02-13 | E-GEOD-51786 | biostudies-arrayexpress

Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [RRBS]

2014-02-13 | GSE52303 | GEO

Premature termination of in vivo reprogramming leads to cancer development through altered epigenetic regulation [array]

2014-02-13 | GSE51786 | GEO

Fibroblast-specific reduction of heparan sulfate suppresses colon tumor growth in mice

Project description:we examined how HS-reduced fibroblasts are involved in the proliferation of colon cancer by using mice in which Ext-1 expression is specifically suppressed in fibroblasts.

2022-06-13 | GSE203597 | GEO

Mthfd1 is a modifier of intestinal carcinogenesis

Project description:The metabolic pathways that underlie the association between folate deficiency and increased risk for colorectal cancer (CRC) remain unclear. We have studied the effect of C1THF synthase (encoded by the Mthfd1 gene) and dietary folate and choline on intestinal tumor development in Apcmin/+ mice and azoxymethane (AOM)-induced colon cancer in mice. Mthfd1 deficiency did not alter tumor number or load in Apcmin/+ mice, but did result in a decreased incidence of colon tumors. Conversely, Mthfd1 deficiency increased tumor number 3.5-fold and tumor load 2-fold in AOM-treated mice. Here we tested colons isolated from wildtype and Mthfd1-deficient animals for alterations in gene expression. Keywords: genetic modification RNA was isolated from proximal colons of MTHFD heterozygous and wild-type mice raised on a control diet. Three colon samples were isolated from each genotype to provide biological replication.

2010-03-20 | E-GEOD-15419 | biostudies-arrayexpress

Mthfd1 is a modifier of intestinal carcinogenesis

2010-03-20 | GSE15419 | GEO

Alterations of DNA methylome during chemical carcinogenesis

Project description:Similar to other genotoxic polycyclic aromatic hydrocarbons (PAHs), benzo[a]pyrene (BaP) is known to produce stable DNA adducts and other DNA damage. BaP is a powerful carcinogen and can induce tumors in the accessory sex organs (including prostate) of rodents. In the present study, we have investigated the potential role of BaP as an epimutagen in vivo during chemical carcinogenesis. We have analyzed the DNA methylation profile, genome-wide, of seminal vesicles of Big Blue® mice exposed to chronic doses of BaP over a period of 6 weeks, both immediately after the termination of exposure and several weeks after-treatment in mice that have developed tumors on the accessory sex organs. Mice treated with chronic doses of DMSO (sham) were used as control.

2013-06-30 | GSE41422 | GEO

Alterations of DNA methylome during chemical carcinogenesis

2013-06-30 | E-GEOD-41422 | biostudies-arrayexpress

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