Article: Identification of a novel function of Id-1 in mediating the anticancer responses of SAMC, a water-soluble garlic derivative, in human bladder cancer cells

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TitleIdentification of a novel function of Id-1 in mediating the anticancer responses of SAMC, a water-soluble garlic derivative, in human bladder cancer cells
AuthorsHu, H1 2
Zhang, XP2
Wang, YL2
Chua, CW1
Luk, SU1
Wong, YC1
Ling, MT1
Wang, XF2
Xu, KX2
Issue Date2011
CitationMolecular Medicine Reports, 2011, v. 4 n. 1, p. 9-16 [How to Cite?]
DOI: http://dx.doi.org/10.3892/mmr.2010.380
AbstractStudies have shown that the expression of inhibitor of differentiation (Id-1) is increased in bladder cancer and is associated with drug resistance. S-allylmercaptocysteine (SAMC), a water-soluble component of garlic, is known to have a potent therapeutic effect on human cancer. The aim of this study was to investigate whether Id-1 expression mediates SAMC-induced cell death in bladder cancer cells. After generating stable Id-1-expressing and si-Id-1 transfectants in various bladder cancer cell lines, cell sensitivity to SAMC was compared by colony formation and MTT assays. The results indicated that Id-1 overexpression reduced the positive effect of SAMC on cell survival, while the inactivation of Id-1 increased cellular susceptibility to SAMC. Using DAPI staining, the apoptosis of bladder cancer cells induced by SAMC was shown to be negatively regulated by Id-1 expression. The expression of apoptosis-related proteins analyzed by Western blotting further supported the negative role of Id-1 in SAMC-induced apoptosis. Furthermore, by wound closure and type I collagen invasion assays, the inhibitory effect of SAMC on the invasion and migration of bladder cancer cells was found to be associated with the down-regulation of Id-1. Our results demonstrated that SAMC-induced apoptosis is associated with the Id-1 pathway, and that the inactivation of Id-1 enhances the ability of SAMC to inhibit the survival, invasion and migration of bladder cancer cells. These findings may lead to the development of novel therapeutic strategies for the treatment of bladder cancer.
ISSN1791-2997
2011 Impact Factor: 0.418
2011 SCImago Journal Rankings: 0.041
DOIhttp://dx.doi.org/10.3892/mmr.2010.380
ISI Accession Number IDWOS:000286301100002
Funding AgencyGrant Number
Peking University People's HospitalRDB2008-30
Funding Information:

This study was supported by the Peking University People's Hospital Research and Development Fund to Dr Ke Xin Xu (RDB2008-30).

ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorHu, H
dc.contributor.authorZhang, XP
dc.contributor.authorWang, YL
dc.contributor.authorChua, CW
dc.contributor.authorLuk, SU
dc.contributor.authorWong, YC
dc.contributor.authorLing, MT
dc.contributor.authorWang, XF
dc.contributor.authorXu, KX
dc.date.accessioned2012-06-26T05:58:09Z
dc.date.available2012-06-26T05:58:09Z
dc.date.issued2011
dc.description.abstractStudies have shown that the expression of inhibitor of differentiation (Id-1) is increased in bladder cancer and is associated with drug resistance. S-allylmercaptocysteine (SAMC), a water-soluble component of garlic, is known to have a potent therapeutic effect on human cancer. The aim of this study was to investigate whether Id-1 expression mediates SAMC-induced cell death in bladder cancer cells. After generating stable Id-1-expressing and si-Id-1 transfectants in various bladder cancer cell lines, cell sensitivity to SAMC was compared by colony formation and MTT assays. The results indicated that Id-1 overexpression reduced the positive effect of SAMC on cell survival, while the inactivation of Id-1 increased cellular susceptibility to SAMC. Using DAPI staining, the apoptosis of bladder cancer cells induced by SAMC was shown to be negatively regulated by Id-1 expression. The expression of apoptosis-related proteins analyzed by Western blotting further supported the negative role of Id-1 in SAMC-induced apoptosis. Furthermore, by wound closure and type I collagen invasion assays, the inhibitory effect of SAMC on the invasion and migration of bladder cancer cells was found to be associated with the down-regulation of Id-1. Our results demonstrated that SAMC-induced apoptosis is associated with the Id-1 pathway, and that the inactivation of Id-1 enhances the ability of SAMC to inhibit the survival, invasion and migration of bladder cancer cells. These findings may lead to the development of novel therapeutic strategies for the treatment of bladder cancer.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationMolecular Medicine Reports, 2011, v. 4 n. 1, p. 9-16 [How to Cite?]
DOI: http://dx.doi.org/10.3892/mmr.2010.380
dc.identifier.doihttp://dx.doi.org/10.3892/mmr.2010.380
dc.identifier.epage16
dc.identifier.isiWOS:000286301100002
Funding AgencyGrant Number
Peking University People's HospitalRDB2008-30
Funding Information:

This study was supported by the Peking University People's Hospital Research and Development Fund to Dr Ke Xin Xu (RDB2008-30).

dc.identifier.issn1791-2997
2011 Impact Factor: 0.418
2011 SCImago Journal Rankings: 0.041
dc.identifier.issue1
dc.identifier.pmid21461556
dc.identifier.scopuseid_2-s2.0-78651404249
dc.identifier.spage9
dc.identifier.urihttp://hdl.handle.net/10722/149757
dc.identifier.volume4
dc.languageeng
dc.relation.ispartofMolecular Medicine Reports
dc.relation.referencesReferences in Scopus
dc.subject.meshAntineoplastic Agents, Phytogenic - Pharmacology
dc.subject.meshCell Death - Drug Effects
dc.subject.meshCell Line, Tumor
dc.subject.meshCell Movement - Drug Effects
dc.subject.meshCysteine - Analogs & Derivatives - Pharmacology
dc.subject.meshGarlic - Chemistry
dc.subject.meshGene Expression Regulation, Neoplastic
dc.subject.meshHumans
dc.subject.meshInhibitor Of Differentiation Protein 1 - Genetics - Metabolism
dc.subject.meshUrinary Bladder Neoplasms - Drug Therapy - Genetics
dc.titleIdentification of a novel function of Id-1 in mediating the anticancer responses of SAMC, a water-soluble garlic derivative, in human bladder cancer cells
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Peking University