Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression profile of butyrate mediated prevention of coloractal cancer in a mouse model

ABSTRACT: To further elucidate the mechanism of butyrate mediated chemoprevention of colorectal cancer,we have employed whole genome microarray expression profiling as a discovery platform to identify genes that differentially expressed in mice from Butyrate group compared those from DMH group. The mice of DMH group were received normal diet (calcium concentration,1.24%) and subcutaneous injection of 1,2-Dimethylhydrazine at a dose of 20 mg/kg once weekly for 20 weeks; the mice of Butyrate group were received high calcium diet (calcium concentration,3%) with 1.5% Butyrate and subcutaneous injection of 1,2-Dimethylhydrazine at a dose of 20 mg/kg once weekly for 20 weeks. The mice were sarcrificed at 24 week. Nine normal colonic mucosa (3 from DMH group, 3 from Butyrate group mice with tumors, and 3 from Butyrate group mice without tumors) were used for the microarray analysis. The differentially expressed genes were identified between butyrate group and DMH group,as long as differentially expressed pathways and gene ontology terms.

ORGANISM(S): Mus musculus

SUBMITTER: Jing-Yuan Fang

PROVIDER: E-GEOD-25858 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:K-ras mutations are observed in around 40% human colorectal adenomas and carcinomas and contribute to the pathogenesis of human and rodent colorectal tumour formation. Previously, we developed and characterised a strain of transgenic mice with inducible intestinal epithelial expression of K-rasVal12 via a Cre/LoxP system. To evaluate the influence of mutant K-ras on carcinogen-induced colorectal tumourigenesis, we induced neoplastic alterations in the large intestines of wild-type and K-rasVal12 mice using the colon-selective carcinogen 1, 2-dimethylhydrazine (DMH), which has been widely used to study chemically induced colorectal tumours that are histopathologically similar to those observed in humans. K-rasVal12 expression significantly promoted DMH-induced colorectal tumourigenesis: the average life span of the mice decreased from 38.52Â±1.97 weeks for 40 wild-type mice to 32.42Â±2.17 weeks for 26 K-rasVal12 mice (mean+SEM, P<0.05) and the large intestinal tumours increased from 2.27Â±0.15 per wild-type mouse to 3.85Â±0.20 in K-rasVal12 mice (mean+SEM, P<0.01). Adenomas from DMH-treated K-rasVal12 mice showed significantly higher levels (10.9Â±1.69%) of Ki-67-positive proliferating cells compared with those from DMH-treated wild-type mice (7.77Â±1.15%) (mean+SD, P<0.01) and a mild increase in apoptotic nuclei staining for cleaved caspase-3 (1.94+0.51% compared with 1.15Â±0.34%, mean+SD, P<0.01). In the adenomas from DMH-treated K-rasVal12 mice, K-rasVal12 transgene recombination and expression were confirmed and shown to promote strong Erk and mild Akt activation compared with adenomas from DMH-treated wild-type mice. Microarray hybridization and cluster analysis demonstrated different expression profiles in adenomas from DMH-treated wild-type and DMH-treated K-rasVal12 mice, indicating involvement of different molecular mechanisms, but array-comparative genomic hybridisation analysis showed chromosome stability in both, with very few chromosome alterations observed in adenomas from either of the two groups. Taken together, these data show that mutant K-ras promotes DMH-induced colorectal tumourigenesis, conferring a proliferative effect, but does not alter chromosome stability in the tumours. This study has 7 samples analysed, 4 Kras mutants and 3 controls, on the Illumina Mouse-6 Beadchip array.

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Gene expression profile of butyrate mediated prevention of coloractal cancer in a mouse model

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