Androgen signaling and post-transcriptional downregulation of Bcl-2 in androgen-unresponsive prostate cancer

C. A. Ruthermun, V. K. Gopalakrishnan, J. K. Vishwanatha

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5 Scopus citations


We previously characterized the LNCaP prostate cancer progression model and showed that despite loss of Bcl-2 protein in the androgen-unresponsive LNCaP-unresponsive (UR) cells, these cells maintained an increased resistance to the induction of apoptosis. Since the loss of Bcl-2 protein coincided with the progression to androgen-unresponsiveness, we sought to determine if Bcl-2 expression was regulated through androgen signaling pathways. LNCaP-responsive (R) and -UR cells grown in charcoal-stripped serum conditions for 3 months differentiated to a neuroendocrine (NE)-like morphology. Under these conditions, LNCaP-UR cells regained Bcl-2 protein expression, and LNCaP-R cells overexpressed Bcl-2. Chronic exposure to casodex resulted in differentiation of both LNCaP-R and -UR cells to the NE-type morphology accompanied by a marked downregulation of Bcl-2 protein, while Bax protein levels were unchanged. Downregulation of Bcl-2 was post-transcriptional since Bcl-2 message levels were unchanged in LNCaP cells treated with casodex. These data suggest that Bcl-2 is post-transcriptionally modulated by androgen signaling pathways in LNCaP cells.

Original languageEnglish
Pages (from-to)158-164
Number of pages7
JournalProstate Cancer and Prostatic Diseases
Issue number2
StatePublished - 2004


  • Androgen-unresponsive
  • Apoptosis
  • Bcl-2 post-transcriptional
  • Casodex
  • Neuroendocrine


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