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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

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
Authors
Issue Date2011
Citation
Molecular Medicine Reports, 2011, v. 4 n. 1, p. 9-16 How to Cite?
Abstract
Studies 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.
Persistent Identifierhttp://hdl.handle.net/10722/149757
ISSN
2013 Impact Factor: 1.484
ISI Accession Number ID
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).

References

 

DC FieldValueLanguage
dc.contributor.authorHu, Hen_US
dc.contributor.authorZhang, XPen_US
dc.contributor.authorWang, YLen_US
dc.contributor.authorChua, CWen_US
dc.contributor.authorLuk, SUen_US
dc.contributor.authorWong, YCen_US
dc.contributor.authorLing, MTen_US
dc.contributor.authorWang, XFen_US
dc.contributor.authorXu, KXen_US
dc.date.accessioned2012-06-26T05:58:09Z-
dc.date.available2012-06-26T05:58:09Z-
dc.date.issued2011en_US
dc.identifier.citationMolecular Medicine Reports, 2011, v. 4 n. 1, p. 9-16en_US
dc.identifier.issn1791-2997en_US
dc.identifier.urihttp://hdl.handle.net/10722/149757-
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.en_US
dc.languageengen_US
dc.relation.ispartofMolecular Medicine Reportsen_US
dc.subject.meshAntineoplastic Agents, Phytogenic - Pharmacologyen_US
dc.subject.meshCell Death - Drug Effectsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Movement - Drug Effectsen_US
dc.subject.meshCysteine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshGarlic - Chemistryen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshHumansen_US
dc.subject.meshInhibitor Of Differentiation Protein 1 - Genetics - Metabolismen_US
dc.subject.meshUrinary Bladder Neoplasms - Drug Therapy - Geneticsen_US
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 cellsen_US
dc.typeArticleen_US
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_US
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_US
dc.identifier.authorityWong, YC=rp00316en_US
dc.identifier.authorityLing, MT=rp00449en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.3892/mmr.2010.380en_US
dc.identifier.pmid21461556en_US
dc.identifier.scopuseid_2-s2.0-78651404249en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78651404249&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume4en_US
dc.identifier.issue1en_US
dc.identifier.spage9en_US
dc.identifier.epage16en_US
dc.identifier.isiWOS:000286301100002-
dc.identifier.scopusauthoridHu, H=36812244900en_US
dc.identifier.scopusauthoridZhang, XP=47461852800en_US
dc.identifier.scopusauthoridWang, YL=47461691100en_US
dc.identifier.scopusauthoridChua, CW=9437494600en_US
dc.identifier.scopusauthoridLuk, SU=36981977600en_US
dc.identifier.scopusauthoridWong, YC=7403041798en_US
dc.identifier.scopusauthoridLing, MT=7102229780en_US
dc.identifier.scopusauthoridWang, XF=34873964600en_US
dc.identifier.scopusauthoridXu, KX=7403282051en_US

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