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Article: Physalins A and B inhibit androgen-independent prostate cancer cell growth through activation of cell apoptosis and downregulation of androgen receptor expression

TitlePhysalins A and B inhibit androgen-independent prostate cancer cell growth through activation of cell apoptosis and downregulation of androgen receptor expression
Authors
KeywordsAndrogen Receptor
Androgen-Independent Prostate Cancer
Apoptosis
Physalin A
Physalin B
Issue Date2011
PublisherPharmaceutical Society of Japan. The Journal's web site is located at http://bpb.pharm.or.jp/index.html
Citation
Biological And Pharmaceutical Bulletin, 2011, v. 34 n. 10, p. 1584-1588 How to Cite?
AbstractAndrogen 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). © 2011 Pharmaceutical Society of Japan.
Persistent Identifierhttp://hdl.handle.net/10722/149768
ISSN
2015 Impact Factor: 1.574
2015 SCImago Journal Rankings: 0.644
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHan, Hen_US
dc.contributor.authorQiu, Len_US
dc.contributor.authorWang, Xen_US
dc.contributor.authorQiu, Fen_US
dc.contributor.authorWong, Yen_US
dc.contributor.authorYao, Xen_US
dc.date.accessioned2012-06-26T05:58:18Z-
dc.date.available2012-06-26T05:58:18Z-
dc.date.issued2011en_US
dc.identifier.citationBiological And Pharmaceutical Bulletin, 2011, v. 34 n. 10, p. 1584-1588en_US
dc.identifier.issn0918-6158en_US
dc.identifier.urihttp://hdl.handle.net/10722/149768-
dc.description.abstractAndrogen 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). © 2011 Pharmaceutical Society of Japan.en_US
dc.languageengen_US
dc.publisherPharmaceutical Society of Japan. The Journal's web site is located at http://bpb.pharm.or.jp/index.htmlen_US
dc.relation.ispartofBiological and Pharmaceutical Bulletinen_US
dc.subjectAndrogen Receptoren_US
dc.subjectAndrogen-Independent Prostate Canceren_US
dc.subjectApoptosisen_US
dc.subjectPhysalin Aen_US
dc.subjectPhysalin Ben_US
dc.titlePhysalins A and B inhibit androgen-independent prostate cancer cell growth through activation of cell apoptosis and downregulation of androgen receptor expressionen_US
dc.typeArticleen_US
dc.identifier.emailWong, Y:ycwong@hkucc.hku.hken_US
dc.identifier.authorityWong, Y=rp00316en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1248/bpb.34.1584en_US
dc.identifier.pmid21963499-
dc.identifier.scopuseid_2-s2.0-80053507350en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80053507350&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume34en_US
dc.identifier.issue10en_US
dc.identifier.spage1584en_US
dc.identifier.epage1588en_US
dc.identifier.isiWOS:000295391100010-
dc.publisher.placeJapanen_US
dc.identifier.scopusauthoridHan, H=24477301600en_US
dc.identifier.scopusauthoridQiu, L=24576884500en_US
dc.identifier.scopusauthoridWang, X=53882069000en_US
dc.identifier.scopusauthoridQiu, F=35235136300en_US
dc.identifier.scopusauthoridWong, Y=7403041798en_US
dc.identifier.scopusauthoridYao, X=35075481900en_US

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