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Cited 23 time in webofscience Cited 23 time in scopus
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dc.contributor.authorLee, Y-
dc.contributor.authorKim, H-
dc.contributor.authorLee, J-
dc.contributor.authorKim, K-
dc.date.accessioned2015-06-25T01:32:47Z-
dc.date.available2015-06-25T01:32:47Z-
dc.date.created2011-06-07-
dc.date.issued2011-05-
dc.identifier.issn0918-6158-
dc.identifier.other2015-OAK-0000023640en_US
dc.identifier.urihttps://oasis.postech.ac.kr/handle/2014.oak/9822-
dc.description.abstractAllylmercapto glutathione S-conjugate, S-allylmercapto-L-cysteine (SAMC), which is biotransformed from allyl sulfides and from naturally occurring water-soluble garlic derivatives, has been known to inhibit tumorigenesis. We found that SAMC was able to induce apoptosis in gastric cancer cells in vitro. We report that SAMC inhibited tumor growth rate by 31.36% and 37.78% at doses of 100 and 300 mg/kg, respectively. Apoptosis in the implanted tumor cells was manifested by apoptotic characteristics, including morphological changes of chromatin crescent, cell shrinkage and membrane blebbing. The apoptosis index of 100 mg/kg and 300 mg/kg of SAMC was 20.74 +/- 2.50% and 30.61 +/- 2.42%, respectively, by terminal deoxy-nucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP) nick-end labeling (TUNEL) staining. The positive rate of B-cell lymphoma 2 (bcl-2) protein expression of control, 100 mg/kg SAMC and 300 mg/kg SAMC was 15.20 +/- 1.67%, 10.94 +/- 1.57%, and 8.24 +/- 1.07%, respectively, by immunohistochemical staining. The positive rate of bax protein expression of control, 100 mg/kg SAMC and 300 mg/kg SAMC was 15.30 +/- 1.90%, 23.18 +/- 1.81%, and 25.26 +/- 3.03%, respectively. We also observed decreases in bcl-2 mRNA and increases in bax mRNA by SAMC in a dose-dependent manner by reverse transcription-polymerase chain reaction (RT-PCR). These results suggest that SAMC may regulate bcl-2 and bax to induce apoptosis in transplanted tumor cells.-
dc.description.statementofresponsibilityopenen_US
dc.languageEnglish-
dc.publisherPHARMACEUTICAL SOC JAPAN-
dc.relation.isPartOfBIOLOGICAL & PHARMACEUTICAL BULLETIN-
dc.rightsBY_NC_NDen_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/2.0/kren_US
dc.titleAnticancer Activity of S-Allylmercapto-L-cysteine on Implanted Tumor of Human Gastric Cancer Cell-
dc.typeArticle-
dc.contributor.college융합생명공학부en_US
dc.identifier.doi10.1248/bpb.34.677-
dc.author.googleLee, Yen_US
dc.author.googleKim, Hen_US
dc.author.googleKim, Ken_US
dc.author.googleLee, Jen_US
dc.relation.volume34en_US
dc.relation.issue5en_US
dc.relation.startpage677en_US
dc.relation.lastpage681en_US
dc.contributor.id10104775en_US
dc.relation.journalBIOLOGICAL & PHARMACEUTICAL BULLETINen_US
dc.relation.indexSCI급, SCOPUS 등재논문en_US
dc.relation.sciSCIen_US
dc.collections.nameJournal Papersen_US
dc.type.rimsART-
dc.identifier.bibliographicCitationBIOLOGICAL & PHARMACEUTICAL BULLETIN, v.34, no.5, pp.677 - 681-
dc.identifier.wosid000290196900013-
dc.date.tcdate2019-01-01-
dc.citation.endPage681-
dc.citation.number5-
dc.citation.startPage677-
dc.citation.titleBIOLOGICAL & PHARMACEUTICAL BULLETIN-
dc.citation.volume34-
dc.contributor.affiliatedAuthorKim, K-
dc.identifier.scopusid2-s2.0-79955671060-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.wostc15-
dc.type.docTypeArticle-
dc.subject.keywordPlusINDUCED APOPTOSIS-
dc.subject.keywordPlusPROSTATE-CANCER-
dc.subject.keywordPlusBCL-2-
dc.subject.keywordPlusBAX-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusRELEASE-
dc.subject.keywordPlusTISSUES-
dc.subject.keywordPlusSULFUR-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthorS-allylmercapto-L-cysteine-
dc.subject.keywordAuthortumor cell-
dc.subject.keywordAuthorbax protein-
dc.subject.keywordAuthorB-cell lymphoma 2 protein-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaPharmacology & Pharmacy-

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김경태KIM, KYONG TAI
Dept of Life Sciences
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