Clusterin expression is significantly enhanced in prostate cancer cells following androgen withdrawal therapy

Progression of prostate cancer to androgen independence (AI) results in part from the upregulation of anti‐apoptotic genes following androgen withdrawal, and androgen‐independent disease remains the primary obstacle to improved survival. Testosterone‐repressed prostate message‐2 (TRPM‐2) encodes the anti‐apoptotic protein clusterin, which is upregulated in response to cellular compromise as observed in normal and malignant tissues undergoing apoptosis. Systemic administration of antisense clusterin oligonucleotides in prostate cancer xenograft models delays progression to AI and enhances chemosensitivity. The objective of this study was to define changes in clusterin expression following neoadjuvant hormone therapy (NHT) in prostate cancer patients.

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