Physalins A and B Inhibit Androgen-Independent Prostate Cancer Cell Growth through Activation of Cell Apoptosis and Downregulation of Androgen Receptor Expression

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概要

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• 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).

著者

• Yao Xinsheng

  College Of Traditional Chinese Materia Medica Shenyang Pharmaceutical University:shenzhen Research C

• Han Huiying

  Extracellular Matrix Pathology Section, Radiation Oncology Branch, Center for Cancer Research, Natio

• Qiu Li

  Guangxi Institute of Medical Plant

• Wang Xianghong

  Cancer Biology Group, Department of Anatomy, Faculty of Medicine, The University of Hong Kong

• Qiu Feng

  College of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University

• Wong Yongchuan

  Cancer Biology Group, Department of Anatomy, Faculty of Medicine, The University of Hong Kong

• Wang Xianghong

  Cancer Biology Group Department Of Anatomy Faculty Of Medicine The University Of Hong Kong

• Han Huiying

  Extracellular Matrix Pathology Section, Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), U.S.A.

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• Physalins A and B Inhibit Androgen-Independent Prostate Cancer Cell Growth through Activation of Cell Apoptosis and Downregulation of Androgen Receptor Expression
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• Evidence of a novel antiapoptotic factor : Role of inhibitor of differentiation or DNA binding (Id-1) in anticancer drug-induced apoptosis

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