physalin-b and Prostatic-Neoplasms

Androgen deprivation therapy is a common treatment strategy for advanced prostate cancer. Though effective initially, the tumor often progresses to androgen independent stage in most patients eventually after a period of remission. One of the key factors of development of resistance is reflected in expression of androgen receptor (AR). In this study, we showed that two natural compounds, physalins A and B, both secosteriods from Physalisalkekengi var. franchetii, significantly inhibited the growth of two androgen-independent cell lines CWR22Rv1 and C42B, induced apoptosis via c-Jun N-terminal kinase (JNK) and/or extracellular signal-regulated kinase (ERK) activation, and decreased AR expression. In addition, physalins A and B down-regulated the expression of prostate specific antigen (PSA) in C42B cells which is a target gene of AR. Our results suggest that physalin A and B might be useful agents in preventing the growth of androgen-independent prostate cancer (AI-PCa).

Topics: Androgen Antagonists; Androgens; Apoptosis; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Down-Regulation; Drug Evaluation, Preclinical; Drug Resistance, Neoplasm; Extracellular Signal-Regulated MAP Kinases; Gene Expression; Gene Expression Regulation, Neoplastic; Humans; JNK Mitogen-Activated Protein Kinases; Male; Molecular Targeted Therapy; Physalis; Phytotherapy; Plant Preparations; Prostate-Specific Antigen; Prostatic Neoplasms; Receptors, Androgen; Secosteroids; Signal Transduction