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Article: A novel anticancer effect of garlic derivatives: Inhibition of cancer cell invasion through restoration of E-cadherin expression

TitleA novel anticancer effect of garlic derivatives: Inhibition of cancer cell invasion through restoration of E-cadherin expression
Authors
Issue Date2006
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2006, v. 27 n. 11, p. 2180-2189 How to Cite?
AbstractMetastatic cancer is one of the main causes of cancer-related death since they rarely respond to available treatments. Recently, certain compounds isolated from the dietary supplement, garlic, have shown anti-proliferation effect on cancer cells. The aim of this study was to investigate whether certain garlic derivatives had any effect on the potentially invasive androgen-independent prostate cancer (PCa) cells. Using colony-forming, wound-closure as well as matrigel-invasion assays, we found that two main water-soluble constituents of the garlic, S-allylcysteine (SAC) and S-allylmercaptocysteine (SAMC), were able to suppress PCa cell proliferation and invasive abilities. This inhibitory effect was associated with induction of mesenchymal to epithelial transition. Most importantly, the SAC and SAMC treatment led to restoration of E-cadherin expression at transcription and protein levels. In contrast, the expression of E-cadherin repressor, Snail, was reduced in the SAC- and SAMC-treated cells. Furthermore, examination of cell lines from other types of cancer (ovarian, nasopharyngeal and esophageal carcinomas) also confirmed that the effect of SAC and SAMC on activation of E-cadherin might be a general effect on human cancer cells. Our results demonstrate a novel anticancer effect of garlic and suggest that certain garlic-derived compounds may be potential agents for suppression of invasive growth through restoration of E-cadherin expression in cancer cells. © 2006 Oxford University Press.
Persistent Identifierhttp://hdl.handle.net/10722/67811
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References
Errata

 

DC FieldValueLanguage
dc.contributor.authorChu, Qen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorFeng, Hen_HK
dc.contributor.authorCheung, HWen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-06T05:58:28Z-
dc.date.available2010-09-06T05:58:28Z-
dc.date.issued2006en_HK
dc.identifier.citationCarcinogenesis, 2006, v. 27 n. 11, p. 2180-2189en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67811-
dc.description.abstractMetastatic cancer is one of the main causes of cancer-related death since they rarely respond to available treatments. Recently, certain compounds isolated from the dietary supplement, garlic, have shown anti-proliferation effect on cancer cells. The aim of this study was to investigate whether certain garlic derivatives had any effect on the potentially invasive androgen-independent prostate cancer (PCa) cells. Using colony-forming, wound-closure as well as matrigel-invasion assays, we found that two main water-soluble constituents of the garlic, S-allylcysteine (SAC) and S-allylmercaptocysteine (SAMC), were able to suppress PCa cell proliferation and invasive abilities. This inhibitory effect was associated with induction of mesenchymal to epithelial transition. Most importantly, the SAC and SAMC treatment led to restoration of E-cadherin expression at transcription and protein levels. In contrast, the expression of E-cadherin repressor, Snail, was reduced in the SAC- and SAMC-treated cells. Furthermore, examination of cell lines from other types of cancer (ovarian, nasopharyngeal and esophageal carcinomas) also confirmed that the effect of SAC and SAMC on activation of E-cadherin might be a general effect on human cancer cells. Our results demonstrate a novel anticancer effect of garlic and suggest that certain garlic-derived compounds may be potential agents for suppression of invasive growth through restoration of E-cadherin expression in cancer cells. © 2006 Oxford University Press.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsCarcinogenesis. Copyright © Oxford University Press.en_HK
dc.subject.meshAntineoplastic Agents - therapeutic useen_HK
dc.subject.meshCadherins - biosynthesisen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Movementen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshCollagen - chemistryen_HK
dc.subject.meshCysteine - analogs & derivatives - chemistry - therapeutic useen_HK
dc.subject.meshDrug Combinationsen_HK
dc.subject.meshDrug Designen_HK
dc.subject.meshGarlicen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInhibitory Concentration 50en_HK
dc.subject.meshLaminin - chemistryen_HK
dc.subject.meshNeoplasm Invasivenessen_HK
dc.subject.meshNeoplasms - drug therapyen_HK
dc.subject.meshProteoglycans - chemistryen_HK
dc.titleA novel anticancer effect of garlic derivatives: Inhibition of cancer cell invasion through restoration of E-cadherin expressionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=27&issue=11&spage=2180&epage=2189&date=2006&atitle=A+novel+anticancer+effect+of+garlic+derivatives:+inhibition+of+cancer+cell+invasion+through+restoration+of+E-cadherin+expressionen_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/carcin/bgl054en_HK
dc.identifier.pmid16675472en_HK
dc.identifier.scopuseid_2-s2.0-33750442231en_HK
dc.identifier.hkuros127164en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33750442231&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume27en_HK
dc.identifier.issue11en_HK
dc.identifier.spage2180en_HK
dc.identifier.epage2189en_HK
dc.identifier.isiWOS:000241629700005-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.erratumdoi:10.1093/carcin/bgl228-
dc.relation.erratumeid:eid_2-s2.0-33845629073-
dc.identifier.scopusauthoridChu, Q=15047860400en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridFeng, H=7401736336en_HK
dc.identifier.scopusauthoridCheung, HW=7201839381en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.citeulike921311-

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