Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 228, Issue 1-2, Pages 105-110Publisher
KLUWER ACADEMIC PUBL
DOI: 10.1023/A:1013303414460
Keywords
estrogen receptor; stable transfection; ligand; gene expression; growth inhibition; cell cycle arrest
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Funding
- NCI NIH HHS [R01 CA-82739-01] Funding Source: Medline
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The estrogen receptor-alpha (ER-alpha) is a ligand-dependent transcription factor that regulates the growth, differentiation, and development of hormone-responsive target organs. While ER-alpha has been reported to play critical role in the pathogenesis and prognosis of breast and prostate cancers, its possible functional role in regulating prostate cancer cell growth in a ligand-dependent or -independent manner is poorly understood. We addressed this question by stably transfecting wild type (wt) ER-alpha cDNA into an invasive estrogen receptor-negative human prostate cancer cell line ARCaP. We isolated several clonal lines of transfected cells expressing varying levels of ER-alpha. The ectopic expression of wt ER-alpha markedly inhibited the growth of ARCaP cells in vitro in an ER-alpha dose-dependent but ligand-independent manner. Flow cytometric analysis of the wt ER-alpha -transfected ARCaP cells revealed that wt ER-alpha expression arrested cell growth in G1 phase. Our results suggest that ER-alpha may regulate prostate cell growth and participate in the pathogenesis of prostate cancer. ER-alpha may be delivered and expressed ectopically to target prostate cancer progression.
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