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Article: Tubeimoside-1 exerts cytotoxicity in heLa cells Through mitochondrial dysfunction and endoplasmic reticulum stress pathways

TitleTubeimoside-1 exerts cytotoxicity in heLa cells Through mitochondrial dysfunction and endoplasmic reticulum stress pathways
Authors
Issue Date2009
PublisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/journals/jprobs
Citation
Journal Of Proteome Research, 2009, v. 8 n. 3, p. 1585-1593 How to Cite?
AbstractTraditional Chinese herbal medicines are a great source of cancer chemotherapeutic agents. Tubeimoside-1 (TBMS1) is a triterpenoid saponin extracted from Bolbostemma paniculatum (Maxim.) Franquet (Cucurbitaceae), a Chinese herb with anticancer potential named as "Tu Bei Mu". In the present study, we used proteomics to examine the cytotoxic effects of TBMS1 on HeLa cells. Protein profiling of TBMS1-treated HeLa cells revealed profound protein alterations related to energy metabolism and protein synthesis and folding, suggesting that mitochondria and endoplasmic reticulum (ER) play a role in TBMS1-initiated apoptosis. TBMS1 induced the depletion of mitochondrial transmembrane potential (Δψm), leading to the activation of aspase-dependent apoptotic cell death. Unfolded Protein Response (UPR) signaling pathways are also activated after TBMS1 treatment and these changes were accompanied by increased expression of GADD153/CHOP, a transcription factor associated with growth arrest and apoptosis in the event of prolonged ER stress. Salubrinal (Sal), a selective inhibitor for ER stress, partially abrogated the TBMS1-related cell death. These results suggest that TBMS1 exerts cytotoxicity in HeLa cells through both mitochondrial dysfunction and ER stress cell death pathways. © 2009 American Chemical Society.
Persistent Identifierhttp://hdl.handle.net/10722/179130
ISSN
2015 Impact Factor: 4.173
2015 SCImago Journal Rankings: 1.962
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXu, Yen_US
dc.contributor.authorChiu, JFen_US
dc.contributor.authorHe, QYen_US
dc.contributor.authorChen, Fen_US
dc.date.accessioned2012-12-19T09:52:13Z-
dc.date.available2012-12-19T09:52:13Z-
dc.date.issued2009en_US
dc.identifier.citationJournal Of Proteome Research, 2009, v. 8 n. 3, p. 1585-1593en_US
dc.identifier.issn1535-3893en_US
dc.identifier.urihttp://hdl.handle.net/10722/179130-
dc.description.abstractTraditional Chinese herbal medicines are a great source of cancer chemotherapeutic agents. Tubeimoside-1 (TBMS1) is a triterpenoid saponin extracted from Bolbostemma paniculatum (Maxim.) Franquet (Cucurbitaceae), a Chinese herb with anticancer potential named as "Tu Bei Mu". In the present study, we used proteomics to examine the cytotoxic effects of TBMS1 on HeLa cells. Protein profiling of TBMS1-treated HeLa cells revealed profound protein alterations related to energy metabolism and protein synthesis and folding, suggesting that mitochondria and endoplasmic reticulum (ER) play a role in TBMS1-initiated apoptosis. TBMS1 induced the depletion of mitochondrial transmembrane potential (Δψm), leading to the activation of aspase-dependent apoptotic cell death. Unfolded Protein Response (UPR) signaling pathways are also activated after TBMS1 treatment and these changes were accompanied by increased expression of GADD153/CHOP, a transcription factor associated with growth arrest and apoptosis in the event of prolonged ER stress. Salubrinal (Sal), a selective inhibitor for ER stress, partially abrogated the TBMS1-related cell death. These results suggest that TBMS1 exerts cytotoxicity in HeLa cells through both mitochondrial dysfunction and ER stress cell death pathways. © 2009 American Chemical Society.en_US
dc.languageengen_US
dc.publisherAmerican Chemical Society. The Journal's web site is located at http://pubs.acs.org/journals/jprobsen_US
dc.relation.ispartofJournal of Proteome Researchen_US
dc.subject.meshAntineoplastic Agents - Pharmacologyen_US
dc.subject.meshApoptosis - Drug Effects - Physiologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Survival - Drug Effectsen_US
dc.subject.meshDrugs, Chinese Herbal - Pharmacologyen_US
dc.subject.meshElectrophoresis, Gel, Two-Dimensionalen_US
dc.subject.meshEndoplasmic Reticulum - Drug Effects - Physiologyen_US
dc.subject.meshHela Cellsen_US
dc.subject.meshHumansen_US
dc.subject.meshMitochondria - Drug Effects - Physiologyen_US
dc.subject.meshSaponins - Pharmacologyen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshTranscription Factor Chop - Metabolismen_US
dc.subject.meshTriterpenes - Pharmacologyen_US
dc.titleTubeimoside-1 exerts cytotoxicity in heLa cells Through mitochondrial dysfunction and endoplasmic reticulum stress pathwaysen_US
dc.typeArticleen_US
dc.identifier.emailChen, F: sfchen@hku.hken_US
dc.identifier.authorityChen, F=rp00672en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1021/pr801001jen_US
dc.identifier.pmid19215086-
dc.identifier.scopuseid_2-s2.0-65249174521en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65249174521&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume8en_US
dc.identifier.issue3en_US
dc.identifier.spage1585en_US
dc.identifier.epage1593en_US
dc.identifier.isiWOS:000264035000045-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridXu, Y=37035700000en_US
dc.identifier.scopusauthoridChiu, JF=7201501692en_US
dc.identifier.scopusauthoridHe, QY=34770287900en_US
dc.identifier.scopusauthoridChen, F=7404907980en_US

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