Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of human MCF7 breast cancer cell line treated with dioxin and DMSO control

ABSTRACT: MCF7 cells were treated with DMSO or 100 nM Dioxin for 16 hr. Gene expression changes were quantified by microarray analyses. Experiment Overall Design: HU133A and B arrays were used to quantify differences in RNA after treatment with 100 nM dioxin for 16 h. The experiment was repeated 3 times.

ORGANISM(S): Homo sapiens

SUBMITTER: Oliver Hankinson

PROVIDER: E-GEOD-7765 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

A proposed mechanism for the protective effect of dioxin against breast cancer.

Hsu Erin L EL Yoon Diana D Choi Hyun Ho HH Wang Feng F Taylor Robert T RT Chen Natalie N Zhang Ruixue R Hankinson Oliver O

Toxicological sciences : an official journal of the Society of Toxicology 20070521 2

Although it is causative for many types of cancers, experimental and epidemiological evidence suggest that 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) may in fact protect against breast cancer. The mechanism(s) for this protection remain unclear. In an attempt to further elucidate this mechanism, we performed a microarray experiment to identify genes that were modulated upon dioxin treatment. We found that dioxin downregulated the messenger RNAs for the G-protein-coupled receptor, CXCR4, as wel ...[more]

PMID: 17517823

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Project description:The dioxin congener 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes a wide range of toxic effects in rodent species, all of which are mediated by a ligand-dependent transcription-factor, the aryl hydrocarbon receptor (AHR). The Han/Wistar (Kuopio) (H/W) strain shows exceptional resistance to many TCDD-induced toxicities; the LD50 of >9600 µg/kg for H/W rats is higher than for any other wild-type mammal known. We have previously shown that this resistance primarily results from H/W rats expressing a variant AHR isoform that has a substantial portion of the AHR transactivation domain deleted. Despite this large deletion, H/W rats are not entirely refractory to the effects of TCDD; the variant AHR in these animals remains fully competent to up-regulate well-known dioxin-inducible genes. TCDD-sensitive (Long-Evans, L-E) and resistant (H/W) rats were treated with either corn-oil (with or without feed-restriction) or 100 µg/kg TCDD for either four or ten days. Hepatic transcriptional profiling was done using microarrays, and was validated by RT-PCR analysis of 41 genes. . A core set of genes was altered in both strains at all time points tested, including CYP1A1, CYP1A2, CYP1B1, Nqo1, Aldh3a1, Tiparp, Exoc3, and Inmt. Outside this core, the strains differed significantly in the breadth of response: three-fold more genes were altered in L-E than H/W rats. At ten days almost all expressed genes were dysregulated in L-E rats, likely reflecting emerging toxic responses. Far fewer genes were affected by feed-restriction, suggesting that only a minority of the TCDD-induced changes are secondary to the wasting syndrome. Rats from sensitive (Long-Evans, LE) and resistant (Han/Wistar, HW) strains were treated with 100 ug/kg TCDD or corn oil vehicle and sacrificed either 4 or 10 days after treatment. LE control rats were either fed normally or feed-restricted to control for the wasting effects of TCDD treatment. Each treatment group contains four or five animals (biological replicates), each of which was assayed on an individual microarray.

Dataset Information

Transcription profiling of human MCF7 breast cancer cell line treated with dioxin and DMSO control

Publications

A proposed mechanism for the protective effect of dioxin against breast cancer.

Similar Datasets

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