Abstract |
In this study, we aimed to evaluate the relationship between PXR and ABCG2 gene expression patterns induced by proinflammatory cytokines in MCF7 and MCF7/MX breast carcinoma cell lines. The effects of proinflammatory cytokines on ABCG2 and PXR mRNA expression were studied using the real-time polymerase chain reaction method. Significant inductions in the ABCG2 and PXR mRNA levels were observed in MCF7 cells, upon treatment with interleukin-1β and tumor necrosis factor-α, whereas MCF7/MX cells did not significantly respond to the treatment. The results also show that in comparison to MCF7 cell line the basal mRNA expression level of PXR was higher in the MCF7/MX cell line. In conclusion, interleukin-1β and tumor necrosis factor-α induced ABCG2 and PXR mRNAs in the MCF7 breast cancer cell line; no significant changes on expression of the same genes in MCF7/MX cells were observed. This differential effect of the cytokines on two different cell lines seems to be influenced by basal levels of the mRNAs, which are very high in MCF7/MX cells. Similar patterns of induction in PXR and ABCG2 genes suggest a probable relationship between these two factors.
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Authors | Obeid M Malekshah, Ahmad Reza Bahrami, Jalil Tavakol Afshari, Fatemeh Mosaffa, Javad Behravan |
Journal | DNA and cell biology
(DNA Cell Biol)
Vol. 30
Issue 1
Pg. 25-31
(Jan 2011)
ISSN: 1557-7430 [Electronic] United States |
PMID | 20846001
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- ABCG2 protein, human
- ATP Binding Cassette Transporter, Subfamily G, Member 2
- ATP-Binding Cassette Transporters
- Cytokines
- Neoplasm Proteins
- Pregnane X Receptor
- RNA, Messenger
- Receptors, Steroid
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Topics |
- ATP Binding Cassette Transporter, Subfamily G, Member 2
- ATP-Binding Cassette Transporters
(genetics)
- Breast Neoplasms
(genetics, pathology)
- Cell Line, Tumor
- Cell Proliferation
(drug effects)
- Cell Survival
(drug effects)
- Cytokines
(pharmacology)
- Gene Expression Regulation, Neoplastic
(drug effects)
- Humans
- Inflammation
(metabolism)
- Neoplasm Proteins
(genetics)
- Pregnane X Receptor
- RNA, Messenger
(genetics, metabolism)
- Receptors, Steroid
(genetics)
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