Inhibition of constitutive aryl hydrocarbon receptor (AhR) signaling attenuates androgen independent signaling and growth in (C4-2) prostate cancer cells

The aryl hydrocarbon receptor is a member of the basic-helix-loop-helix family of transcription factors. AhR mediates the biochemical and toxic effects of a number of polyaromatic hydrocarbons such as 2,3,7,8,-tetrachloro-dibenzo-p-dioxin (TCDD). AhR is widely known for regulating the transcription...

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Published inBiochemical pharmacology Vol. 85; no. 6; pp. 753 - 762
Main Authors Tran, Cindy, Richmond, Oliver, Aaron, LaTayia, Powell, Joann B.
Format Journal Article
LanguageEnglish
Published England Elsevier Inc 15.03.2013
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Abstract The aryl hydrocarbon receptor is a member of the basic-helix-loop-helix family of transcription factors. AhR mediates the biochemical and toxic effects of a number of polyaromatic hydrocarbons such as 2,3,7,8,-tetrachloro-dibenzo-p-dioxin (TCDD). AhR is widely known for regulating the transcription of drug metabolizing enzymes involved in the xenobiotic metabolism of carcinogens and therapeutic agents, such as cytochrome P450-1B1 (CYP1B1). Additionally, AhR has also been reported to interact with multiple signaling pathways during prostate development. Here we investigate the effect of sustained AhR signaling on androgen receptor function in prostate cancer cells. Immunoblot analysis shows that AhR expression is increased in androgen independent (C4-2) prostate cancer cells when compared to androgen sensitive (LNCaP) cells. RT-PCR studies revealed constitutive AhR signaling in C4-2 cells without the ligand induced activation required in LNCaP cells. A reduction of AhR activity by short RNA mediated silencing in C4-2 cells reduced expression of both AhR and androgen responsive genes. The decrease in androgen responsive genes correlates to a decrease in phosphorylated androgen receptor and androgen receptor expression in the nucleus. Furthermore, the forced decrease in AhR expression resulted in a 50% decline in the growth rate of C4-2 cells. These data indicates that AhR is required to maintain hormone independent signaling and growth by the androgen receptor in C4-2 cells. Collectively, these data provide evidence of a direct role for AhR in androgen independent signaling and provides insight into the molecular mechanisms responsible for sustained androgen receptor signaling in hormone refractory prostate cancer.
AbstractList The aryl hydrocarbon receptor is a member of the basic-helix-loop-helix family of transcription factors. AhR mediates the biochemical and toxic effects of a number of polyaromatic hydrocarbons such as 2,3,7,8,-tetrachloro-dibenzo-p-dioxin (TCDD). AhR is widely known for regulating the transcription of drug metabolizing enzymes involved in the xenobiotic metabolism of carcinogens and therapeutic agents, such as cytochrome P450-1B1 (CYP1B1). Additionally, AhR has also been reported to interact with multiple signaling pathways during prostate development. Here we investigate the effect of sustained AhR signaling on androgen receptor function in prostate cancer cells. Immunoblot analysis shows that AhR expression is increased in androgen independent (C4-2) prostate cancer cells when compared to androgen sensitive (LNCaP) cells. RT-PCR studies revealed constitutive AhR signaling in C4-2 cells without the ligand induced activation required in LNCaP cells. A reduction of AhR activity by short RNA mediated silencing in C4-2 cells reduced expression of both AhR and androgen responsive genes. The decrease in androgen responsive genes correlates to a decrease in phosphorylated androgen receptor and androgen receptor expression in the nucleus. Furthermore, the forced decrease in AhR expression resulted in a 50% decline in the growth rate of C4-2 cells. These data indicates that AhR is required to maintain hormone independent signaling and growth by the androgen receptor in C4-2 cells. Collectively, these data provide evidence of a direct role for AhR in androgen independent signaling and provides insight into the molecular mechanisms responsible for sustained androgen receptor signaling in hormone refractory prostate cancer.
Author Tran, Cindy
Richmond, Oliver
Aaron, LaTayia
Powell, Joann B.
AuthorAffiliation a Center for Cancer Research and Therapeutic Development, Clark Atlanta University, 223 James P. Brawley Drive, Atlanta, GA 30314, United States
b Department of Biological Sciences, Clark Atlanta University, 223 James P. Brawley Drive, Atlanta, GA 30314, United States
AuthorAffiliation_xml – name: b Department of Biological Sciences, Clark Atlanta University, 223 James P. Brawley Drive, Atlanta, GA 30314, United States
– name: a Center for Cancer Research and Therapeutic Development, Clark Atlanta University, 223 James P. Brawley Drive, Atlanta, GA 30314, United States
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  email: jpowell@cau.edu
  organization: Center for Cancer Research and Therapeutic Development, Clark Atlanta University, 223 James P. Brawley Drive, Atlanta, GA 30314, United States
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Keywords Progression
TCDD
AhR
Dioxin
Androgen receptor
Language English
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Snippet The aryl hydrocarbon receptor is a member of the basic-helix-loop-helix family of transcription factors. AhR mediates the biochemical and toxic effects of a...
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SourceType Open Access Repository
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SubjectTerms AhR
Androgen receptor
androgen receptors
Androgens - physiology
Base Sequence
Blotting, Western
carcinogens
Cell Division
Cell Line, Tumor
Cell Proliferation
Dioxin
DNA Primers
drugs
enzymes
genes
Humans
Immunohistochemistry
Male
metabolism
polycyclic aromatic hydrocarbons
Progression
prostatic neoplasms
Prostatic Neoplasms - metabolism
Prostatic Neoplasms - pathology
Receptors, Aryl Hydrocarbon - metabolism
Reverse Transcriptase Polymerase Chain Reaction
RNA
Signal Transduction
TCDD
toxicity
transcription factors
Title Inhibition of constitutive aryl hydrocarbon receptor (AhR) signaling attenuates androgen independent signaling and growth in (C4-2) prostate cancer cells
URI https://dx.doi.org/10.1016/j.bcp.2012.12.010
https://www.ncbi.nlm.nih.gov/pubmed/23266674
https://pubmed.ncbi.nlm.nih.gov/PMC3663294
Volume 85
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