Abstract
The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor. Recent studies have reported the anti-tumor effects of the AhR in breast cancer. In this study, we investigated the anti-tumor effect of AhR activation based on the cancer stem cell hypothesis. We show that AhR activation suppressed mammosphere formation of MCF-7 cells and decreased the proportion of cells with high ALDH-1 (aldehyde dehydrogenase 1) activity. In addition, we also demonstrate that AhR activation regulates self-renewal signaling by down-regulating Wnt/β-catenin and Notch.
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aldehyde Dehydrogenase 1 Family
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Blotting, Western
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Cell Line, Tumor
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Cell Proliferation / drug effects
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Cell Survival / drug effects
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Cytochrome P-450 CYP1A1 / genetics
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Cytochrome P-450 CYP1A1 / metabolism
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Dose-Response Relationship, Drug
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Female
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Gene Expression Regulation, Neoplastic*
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Humans
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Isoenzymes / metabolism
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Methylcholanthrene / pharmacology
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Microscopy, Confocal
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Neoplastic Stem Cells / drug effects
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Neoplastic Stem Cells / metabolism
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Neoplastic Stem Cells / pathology
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RNA Interference
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Receptors, Aryl Hydrocarbon / agonists
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Receptors, Aryl Hydrocarbon / genetics*
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Receptors, Aryl Hydrocarbon / metabolism*
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Receptors, Notch / metabolism
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Retinal Dehydrogenase / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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Spheroids, Cellular / drug effects
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Spheroids, Cellular / metabolism*
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Spheroids, Cellular / pathology
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Wnt Proteins / metabolism
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beta Catenin / metabolism
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beta-Naphthoflavone / pharmacology
Substances
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Isoenzymes
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Receptors, Aryl Hydrocarbon
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Receptors, Notch
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Wnt Proteins
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beta Catenin
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Methylcholanthrene
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beta-Naphthoflavone
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Cytochrome P-450 CYP1A1
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Aldehyde Dehydrogenase 1 Family
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ALDH1A1 protein, human
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Retinal Dehydrogenase