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Article: Proteomic and transcriptomic study on the action of a cytotoxic saponin (Polyphyllin D): Induction of endoplasmic reticulum stress and mitochondria-mediated apoptotic pathways

TitleProteomic and transcriptomic study on the action of a cytotoxic saponin (Polyphyllin D): Induction of endoplasmic reticulum stress and mitochondria-mediated apoptotic pathways
Authors
Issue Date2008
PublisherWiley - V C H Verlag GmbH & Co KGaA. The Journal's web site is located at http://www.wiley-vch.de/home/proteomics
Citation
Proteomics, 2008, v. 8 n. 15, p. 3105-3117 How to Cite?
AbstractPolyphyllin D (PD) is a potent cytotoxic saponin found in Paris polyphylla. In the present study, bioinformatic, proteomic and transcriptomic analyses were performed to study the mechanisms of action of PD on human nonsmall cell lung cancer (NSCLC) cell line (NCI-H460). Using a gene expression-based bioinformatic tool (connectivity map), PD was identified as a potential ER stress inducer. Our proteomic and transcriptomic analyses revealed that PD treatment led to upregulation of typical ER stress-related proteins/genes including glucose-regulated protein 78 (BiP/GRP78) and protein disulfide isomerase (PDI). In particular, elevated expression of C/EBP homologous transcription factor (chop) and activation of caspase-4 occurred at early time point (8 h) of PD treatment, signifying an initial ER stress-mediated apoptosis. Induction of tumor suppressor p53, disruption of mitochondrial membrane, activation of caspase-9 and caspase-3 were detected upon prolonged PD treatment. Collectively, these data revealed that PD induced the cytotoxic effect through a mechanism initiated by ER stress followed by mitochondrial apoptotic pathway. The ability of activating two major pathways of apoptosis makes PD an attractive drug lead for anticancer therapeutics. © 2008 Wiley-VCH Verlag GmbH & Co. KGaA.
Persistent Identifierhttp://hdl.handle.net/10722/168319
ISSN
2015 Impact Factor: 4.079
2015 SCImago Journal Rankings: 1.476
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSiu, FMen_US
dc.contributor.authorMa, DLen_US
dc.contributor.authorCheung, YWen_US
dc.contributor.authorLok, CNen_US
dc.contributor.authorYan, Ken_US
dc.contributor.authorYang, Zen_US
dc.contributor.authorYang, Men_US
dc.contributor.authorXu, Sen_US
dc.contributor.authorKo, BCBen_US
dc.contributor.authorHe, QYen_US
dc.contributor.authorChe, CMen_US
dc.date.accessioned2012-10-08T03:17:29Z-
dc.date.available2012-10-08T03:17:29Z-
dc.date.issued2008en_US
dc.identifier.citationProteomics, 2008, v. 8 n. 15, p. 3105-3117en_US
dc.identifier.issn1615-9853en_US
dc.identifier.urihttp://hdl.handle.net/10722/168319-
dc.description.abstractPolyphyllin D (PD) is a potent cytotoxic saponin found in Paris polyphylla. In the present study, bioinformatic, proteomic and transcriptomic analyses were performed to study the mechanisms of action of PD on human nonsmall cell lung cancer (NSCLC) cell line (NCI-H460). Using a gene expression-based bioinformatic tool (connectivity map), PD was identified as a potential ER stress inducer. Our proteomic and transcriptomic analyses revealed that PD treatment led to upregulation of typical ER stress-related proteins/genes including glucose-regulated protein 78 (BiP/GRP78) and protein disulfide isomerase (PDI). In particular, elevated expression of C/EBP homologous transcription factor (chop) and activation of caspase-4 occurred at early time point (8 h) of PD treatment, signifying an initial ER stress-mediated apoptosis. Induction of tumor suppressor p53, disruption of mitochondrial membrane, activation of caspase-9 and caspase-3 were detected upon prolonged PD treatment. Collectively, these data revealed that PD induced the cytotoxic effect through a mechanism initiated by ER stress followed by mitochondrial apoptotic pathway. The ability of activating two major pathways of apoptosis makes PD an attractive drug lead for anticancer therapeutics. © 2008 Wiley-VCH Verlag GmbH & Co. KGaA.en_US
dc.languageengen_US
dc.publisherWiley - V C H Verlag GmbH & Co KGaA. The Journal's web site is located at http://www.wiley-vch.de/home/proteomicsen_US
dc.relation.ispartofProteomicsen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshCarcinoma, Non-Small-Cell Lung - Genetics - Metabolism - Pathologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshDiosgenin - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshEndoplasmic Reticulum - Metabolismen_US
dc.subject.meshGene Expression Profiling - Methodsen_US
dc.subject.meshGene Expression Regulation, Neoplastic - Drug Effectsen_US
dc.subject.meshHeat-Shock Proteins - Genetics - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshLung Neoplasms - Genetics - Metabolism - Pathologyen_US
dc.subject.meshMitochondria - Metabolismen_US
dc.subject.meshMolecular Chaperones - Genetics - Metabolismen_US
dc.subject.meshProteomics - Methodsen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshTranscription Factor Chop - Genetics - Metabolismen_US
dc.subject.meshTumor Suppressor Protein P53 - Genetics - Metabolismen_US
dc.titleProteomic and transcriptomic study on the action of a cytotoxic saponin (Polyphyllin D): Induction of endoplasmic reticulum stress and mitochondria-mediated apoptotic pathwaysen_US
dc.typeArticleen_US
dc.identifier.emailSiu, FM:fmsiu@hku.hken_US
dc.identifier.emailMa, DL:edmondma@hku.hken_US
dc.identifier.emailLok, CN:cnlok@hku.hken_US
dc.identifier.emailChe, CM:cmche@hku.hken_US
dc.identifier.authoritySiu, FM=rp00776en_US
dc.identifier.authorityMa, DL=rp00760en_US
dc.identifier.authorityLok, CN=rp00752en_US
dc.identifier.authorityChe, CM=rp00670en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/pmic.200700829en_US
dc.identifier.pmid18615425-
dc.identifier.scopuseid_2-s2.0-49749104260en_US
dc.identifier.hkuros147777-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-49749104260&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume8en_US
dc.identifier.issue15en_US
dc.identifier.spage3105en_US
dc.identifier.epage3117en_US
dc.identifier.eissn1615-9861-
dc.identifier.isiWOS:000258503400012-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridSiu, FM=6701518489en_US
dc.identifier.scopusauthoridMa, DL=7402075538en_US
dc.identifier.scopusauthoridCheung, YW=24586913200en_US
dc.identifier.scopusauthoridLok, CN=7006410829en_US
dc.identifier.scopusauthoridYan, K=35340293700en_US
dc.identifier.scopusauthoridYang, Z=13205034800en_US
dc.identifier.scopusauthoridYang, M=7404925734en_US
dc.identifier.scopusauthoridXu, S=24475645200en_US
dc.identifier.scopusauthoridKo, BCB=7102833927en_US
dc.identifier.scopusauthoridHe, QY=34770287900en_US
dc.identifier.scopusauthoridChe, CM=7102442791en_US

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