File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Evidence of a novel docetaxel sensitizer, garlic-derived S-allylmercaptocysteine, as a treatment option for hormone refractory prostate cancer
  • Basic View
  • Metadata View
  • XML View
TitleEvidence of a novel docetaxel sensitizer, garlic-derived S-allylmercaptocysteine, as a treatment option for hormone refractory prostate cancer
 
AuthorsHoward, EW1
Lee, DT1
Yung, TC1
Chee, WC1
Wang, X1
Yong, CW1
 
Issue Date2008
 
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
 
CitationInternational Journal Of Cancer, 2008, v. 122 n. 9, p. 1941-1948 [How to Cite?]
DOI: http://dx.doi.org/10.1002/ijc.23355
 
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.
 
ISSN0020-7136
2013 Impact Factor: 5.007
 
DOIhttp://dx.doi.org/10.1002/ijc.23355
 
ISI Accession Number IDWOS:000254224100004
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorHoward, EW
 
dc.contributor.authorLee, DT
 
dc.contributor.authorYung, TC
 
dc.contributor.authorChee, WC
 
dc.contributor.authorWang, X
 
dc.contributor.authorYong, CW
 
dc.date.accessioned2010-09-06T05:58:46Z
 
dc.date.available2010-09-06T05:58:46Z
 
dc.date.issued2008
 
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.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationInternational Journal Of Cancer, 2008, v. 122 n. 9, p. 1941-1948 [How to Cite?]
DOI: http://dx.doi.org/10.1002/ijc.23355
 
dc.identifier.doihttp://dx.doi.org/10.1002/ijc.23355
 
dc.identifier.epage1948
 
dc.identifier.hkuros147327
 
dc.identifier.isiWOS:000254224100004
 
dc.identifier.issn0020-7136
2013 Impact Factor: 5.007
 
dc.identifier.issue9
 
dc.identifier.openurl
 
dc.identifier.pmid18183597
 
dc.identifier.scopuseid_2-s2.0-40749160978
 
dc.identifier.spage1941
 
dc.identifier.urihttp://hdl.handle.net/10722/67843
 
dc.identifier.volume122
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
 
dc.publisher.placeUnited States
 
dc.relation.ispartofInternational Journal of Cancer
 
dc.relation.referencesReferences in Scopus
 
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.
 
dc.subject.meshAnimals
 
dc.subject.meshAntineoplastic Combined Chemotherapy Protocols - adverse effects - pharmacology
 
dc.subject.meshApoptosis - drug effects
 
dc.subject.meshBlotting, Western
 
dc.subject.meshCadherins - metabolism
 
dc.subject.meshCell Division - drug effects
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshCysteine - adverse effects - analogs & derivatives - pharmacology
 
dc.subject.meshDown-Regulation - drug effects
 
dc.subject.meshDrug Synergism
 
dc.subject.meshFlow Cytometry
 
dc.subject.meshG2 Phase - drug effects
 
dc.subject.meshGarlic
 
dc.subject.meshGene Expression Regulation, Neoplastic - drug effects
 
dc.subject.meshHumans
 
dc.subject.meshImmunohistochemistry
 
dc.subject.meshMale
 
dc.subject.meshMice
 
dc.subject.meshMice, Nude
 
dc.subject.meshNeoplasms, Experimental - drug therapy - metabolism
 
dc.subject.meshProstatic Neoplasms - drug therapy - metabolism
 
dc.subject.meshProto-Oncogene Proteins c-bcl-2 - metabolism
 
dc.subject.meshTaxoids - adverse effects - pharmacology
 
dc.subject.meshTransplantation, Heterologous
 
dc.subject.meshTumor Stem Cell Assay
 
dc.subject.meshUp-Regulation - drug effects
 
dc.titleEvidence of a novel docetaxel sensitizer, garlic-derived S-allylmercaptocysteine, as a treatment option for hormone refractory prostate cancer
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Howard, EW</contributor.author>
<contributor.author>Lee, DT</contributor.author>
<contributor.author>Yung, TC</contributor.author>
<contributor.author>Chee, WC</contributor.author>
<contributor.author>Wang, X</contributor.author>
<contributor.author>Yong, CW</contributor.author>
<date.accessioned>2010-09-06T05:58:46Z</date.accessioned>
<date.available>2010-09-06T05:58:46Z</date.available>
<date.issued>2008</date.issued>
<identifier.citation>International Journal Of Cancer, 2008, v. 122 n. 9, p. 1941-1948</identifier.citation>
<identifier.issn>0020-7136</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/67843</identifier.uri>
<description.abstract>The 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. &#169; 2008 Wiley-Liss, Inc.</description.abstract>
<language>eng</language>
<publisher>John Wiley &amp; Sons, Inc.. The Journal&apos;s web site is located at http://www3.interscience.wiley.com/journal/29331/home</publisher>
<relation.ispartof>International Journal of Cancer</relation.ispartof>
<rights>International Journal of Cancer. Copyright &#169; John Wiley &amp; Sons, Inc.</rights>
<subject.mesh>Animals</subject.mesh>
<subject.mesh>Antineoplastic Combined Chemotherapy Protocols - adverse effects - pharmacology</subject.mesh>
<subject.mesh>Apoptosis - drug effects</subject.mesh>
<subject.mesh>Blotting, Western</subject.mesh>
<subject.mesh>Cadherins - metabolism</subject.mesh>
<subject.mesh>Cell Division - drug effects</subject.mesh>
<subject.mesh>Cell Line, Tumor</subject.mesh>
<subject.mesh>Cysteine - adverse effects - analogs &amp; derivatives - pharmacology</subject.mesh>
<subject.mesh>Down-Regulation - drug effects</subject.mesh>
<subject.mesh>Drug Synergism</subject.mesh>
<subject.mesh>Flow Cytometry</subject.mesh>
<subject.mesh>G2 Phase - drug effects</subject.mesh>
<subject.mesh>Garlic</subject.mesh>
<subject.mesh>Gene Expression Regulation, Neoplastic - drug effects</subject.mesh>
<subject.mesh>Humans</subject.mesh>
<subject.mesh>Immunohistochemistry</subject.mesh>
<subject.mesh>Male</subject.mesh>
<subject.mesh>Mice</subject.mesh>
<subject.mesh>Mice, Nude</subject.mesh>
<subject.mesh>Neoplasms, Experimental - drug therapy - metabolism</subject.mesh>
<subject.mesh>Prostatic Neoplasms - drug therapy - metabolism</subject.mesh>
<subject.mesh>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject.mesh>
<subject.mesh>Taxoids - adverse effects - pharmacology</subject.mesh>
<subject.mesh>Transplantation, Heterologous</subject.mesh>
<subject.mesh>Tumor Stem Cell Assay</subject.mesh>
<subject.mesh>Up-Regulation - drug effects</subject.mesh>
<title>Evidence of a novel docetaxel sensitizer, garlic-derived S-allylmercaptocysteine, as a treatment option for hormone refractory prostate cancer</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0020-7136&amp;volume=122&amp;spage=1941&amp;epage=1948&amp;date=2008&amp;atitle=Evidence+of+a+novel+docetaxel+sensitizer,+garlic-derived+S-allylmercaptocysteine,+as+a+treatment+option+for+hormone+refractory+prostate+cancer</identifier.openurl>
<description.nature>link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1002/ijc.23355</identifier.doi>
<identifier.pmid>18183597</identifier.pmid>
<identifier.scopus>eid_2-s2.0-40749160978</identifier.scopus>
<identifier.hkuros>147327</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-40749160978&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>122</identifier.volume>
<identifier.issue>9</identifier.issue>
<identifier.spage>1941</identifier.spage>
<identifier.epage>1948</identifier.epage>
<identifier.isi>WOS:000254224100004</identifier.isi>
<publisher.place>United States</publisher.place>
</item>
Author Affiliations
  1. The University of Hong Kong