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Article: Evidence of a novel docetaxel sensitizer, garlic-derived S-allylmercaptocysteine, as a treatment option for hormone refractory prostate cancer

TitleEvidence of a novel docetaxel sensitizer, garlic-derived S-allylmercaptocysteine, as a treatment option for hormone refractory prostate cancer
Authors
Issue Date2008
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2008, v. 122 n. 9, p. 1941-1948 How to Cite?
AbstractThe recent introduction of docetaxel in the treatment of hormone refractory prostate cancer (HRPC) has made a small but significant impact on patient survival. However, its effect is limited by intolerance and resistance. The aim of our study was to investigate if the garlic-derived compound, S-allylmercaptocysteine (SAMC), was able to act as a docetaxel sensitizing agent. First, the effect of SAMC on docetaxel sensitivity was examined on 3 HRPC cell lines by colony forming assay. We found that SAMC increased the efficacy of docetaxel on colony forming inhibition by 9-50% compared to single agent treatment. Second, using the HRPC CWR22R nude mice model, we found that the combination of SAMC and docetaxel was 53% more potent than docetaxel alone (p = 0.037). In addition, there was no additive toxicity in the mice treated with the combination therapy evidenced by histological and functional analysis of liver, kidney and bone marrow. These results suggest that SAMC is able to increase the anticancer effect of docetaxel without causing additional toxic effect in vivo. Third, flow cytometry and Western blotting analysis on HRPC cell lines demonstrated that SAMC promoted docetaxel-induced G2/M phase cell cycle arrest and apoptotic induction. In addition, immunohistochemistry on CWR22R xenograft revealed a suppression of Bcl-2 expression and upregulation of E-cadherin in the SAMC and docetaxel treated animals. These results suggest that SAMC may promote docetaxel-induced cell death through promoting G2/M cell cycle arrest and apoptosis. Our study implies a potential role for SAMC in improving docetaxel based chemotherapy for the treatment of HRPC. © 2008 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/67843
ISSN
2014 Impact Factor: 5.085
2014 SCImago Journal Rankings: 2.175
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHoward, EWen_HK
dc.contributor.authorLee, DTen_HK
dc.contributor.authorYung, TCen_HK
dc.contributor.authorChee, WCen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorYong, CWen_HK
dc.date.accessioned2010-09-06T05:58:46Z-
dc.date.available2010-09-06T05:58:46Z-
dc.date.issued2008en_HK
dc.identifier.citationInternational Journal Of Cancer, 2008, v. 122 n. 9, p. 1941-1948en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67843-
dc.description.abstractThe recent introduction of docetaxel in the treatment of hormone refractory prostate cancer (HRPC) has made a small but significant impact on patient survival. However, its effect is limited by intolerance and resistance. The aim of our study was to investigate if the garlic-derived compound, S-allylmercaptocysteine (SAMC), was able to act as a docetaxel sensitizing agent. First, the effect of SAMC on docetaxel sensitivity was examined on 3 HRPC cell lines by colony forming assay. We found that SAMC increased the efficacy of docetaxel on colony forming inhibition by 9-50% compared to single agent treatment. Second, using the HRPC CWR22R nude mice model, we found that the combination of SAMC and docetaxel was 53% more potent than docetaxel alone (p = 0.037). In addition, there was no additive toxicity in the mice treated with the combination therapy evidenced by histological and functional analysis of liver, kidney and bone marrow. These results suggest that SAMC is able to increase the anticancer effect of docetaxel without causing additional toxic effect in vivo. Third, flow cytometry and Western blotting analysis on HRPC cell lines demonstrated that SAMC promoted docetaxel-induced G2/M phase cell cycle arrest and apoptotic induction. In addition, immunohistochemistry on CWR22R xenograft revealed a suppression of Bcl-2 expression and upregulation of E-cadherin in the SAMC and docetaxel treated animals. These results suggest that SAMC may promote docetaxel-induced cell death through promoting G2/M cell cycle arrest and apoptosis. Our study implies a potential role for SAMC in improving docetaxel based chemotherapy for the treatment of HRPC. © 2008 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntineoplastic Combined Chemotherapy Protocols - adverse effects - pharmacologyen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCadherins - metabolismen_HK
dc.subject.meshCell Division - drug effectsen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCysteine - adverse effects - analogs & derivatives - pharmacologyen_HK
dc.subject.meshDown-Regulation - drug effectsen_HK
dc.subject.meshDrug Synergismen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshG2 Phase - drug effectsen_HK
dc.subject.meshGarlicen_HK
dc.subject.meshGene Expression Regulation, Neoplastic - drug effectsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshNeoplasms, Experimental - drug therapy - metabolismen_HK
dc.subject.meshProstatic Neoplasms - drug therapy - metabolismen_HK
dc.subject.meshProto-Oncogene Proteins c-bcl-2 - metabolismen_HK
dc.subject.meshTaxoids - adverse effects - pharmacologyen_HK
dc.subject.meshTransplantation, Heterologousen_HK
dc.subject.meshTumor Stem Cell Assayen_HK
dc.subject.meshUp-Regulation - drug effectsen_HK
dc.titleEvidence of a novel docetaxel sensitizer, garlic-derived S-allylmercaptocysteine, as a treatment option for hormone refractory prostate canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-7136&volume=122&spage=1941&epage=1948&date=2008&atitle=Evidence+of+a+novel+docetaxel+sensitizer,+garlic-derived+S-allylmercaptocysteine,+as+a+treatment+option+for+hormone+refractory+prostate+canceren_HK
dc.identifier.emailYong, CW:ycwong@hkucc.hku.hken_HK
dc.identifier.authorityYong, CW=rp00316en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.23355en_HK
dc.identifier.pmid18183597-
dc.identifier.scopuseid_2-s2.0-40749160978en_HK
dc.identifier.hkuros147327en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-40749160978&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume122en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1941en_HK
dc.identifier.epage1948en_HK
dc.identifier.isiWOS:000254224100004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHoward, EW=16480736900en_HK
dc.identifier.scopusauthoridLee, DT=7406666118en_HK
dc.identifier.scopusauthoridYung, TC=35084586300en_HK
dc.identifier.scopusauthoridChee, WC=16642230300en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridYong, CW=7403041798en_HK

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