title: Physalins A and B inhibit androgen-independent prostate cancer cell growth through activation of cell apoptosis and downregulation of androgen receptor expression.
abstract: 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).
authors.affiliation: Extracellular Matrix Pathology Section, Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892–4605, USA.
authors.forename: Huiying
authors.initials: H
authors.lastname: Han
authors.forename: Li
authors.initials: L
authors.lastname: Qiu
authors.forename: Xianghong
authors.initials: X
authors.lastname: Wang
authors.forename: Feng
authors.initials: F
authors.lastname: Qiu
authors.forename: Yongchuan
authors.initials: Y
authors.lastname: Wong
authors.forename: Xinsheng
authors.initials: X
authors.lastname: Yao
mesh_terms: D000726:Androgen Antagonists / Q000302:isolation & purification / Q000494:pharmacology*; D000728:Androgens / Q000502:physiology*; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D002453:Cell Cycle / Q000187:drug effects / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D015536:Down-Regulation; D004353:Drug Evaluation, Preclinical; D019008:Drug Resistance, Neoplasm; D048049:Extracellular Signal-Regulated MAP Kinases / Q000235:genetics / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D008297:Male; D058990:Molecular Targeted Therapy; D032321:Physalis; D008517:Phytotherapy; D028321:Plant Preparations / Q000302:isolation & purification / Q000494:pharmacology; D017430:Prostate-Specific Antigen / Q000037:antagonists & inhibitors; D011471:Prostatic Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D011944:Receptors, Androgen / Q000502:physiology*; D012632:Secosteroids / Q000302:isolation & purification / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics
chemical_list: D000726:Androgen Antagonists; D000728:Androgens; D028321:Plant Preparations; D011944:Receptors, Androgen; D012632:Secosteroids; C033270:physalin B; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D017430:Prostate-Specific Antigen