Lack of androgen receptor transcriptional activity in human keratinocytes.
Since detection of androgen receptor (AR) expression in keratinocytes by immunostaining is controversial, we investigated whether keratinocytes can act as androgen target cells using transient transfection assays. Chloramphenicol acetyltransferase (CAT) assays for the endogenous AR transcriptional activity in HaCaT keratinocytes indicated that DHT (10(-9)-10(-8) M) can induce less than 1.5-fold of mouse mammary tumor virus CAT, which is quite low, compared with 38-fold induction by 10(-7) M 1,25-dihydroxyvitamin D(3) of P450cc24-CAT. Furthermore, this low DHT-mediated induction could not be enhanced by the AR co-activators, ARA70 or ARA55. Western blotting analysis indicated that HaCaT and normal keratinocytes do not express AR protein. Transfection of exogenous AR into HaCaT keratinocytes, however, could install AR transcriptional activity, suggesting that HaCaT keratinocytes have all the necessary accessory factors for AR transcription activity. In conclusion, keratinocytes are unlikely to be target cells for androgen.
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George Hoyt Whipple Laboratory for Cancer Research, Departments of Pathology and Urology, University of Rochester Medical Center, 601 Elmwood Ave., Box 626, Rochester, NY 14642, USA.
Itami
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Pan
H J
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Chang
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D000818:Animals; D002460:Cell Line; D015500:Chloramphenicol O-Acetyltransferase / Q000235:genetics; D013196:Dihydrotestosterone / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects; D017930:Genes, Reporter; D006801:Humans; D015603:Keratinocytes / Q000378:metabolism*; D008324:Mammary Tumor Virus, Mouse / Q000235:genetics; D051379:Mice; D011944:Receptors, Androgen / Q000378:metabolism*; D014158:Transcription, Genetic / Q000187:drug effects; D014162:Transfection
D011944:Receptors, Androgen; D013196:Dihydrotestosterone; D015500:Chloramphenicol O-Acetyltransferase