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Article: Protein alterations associated with temozolomide resistance in subclones of human glioblastoma cell lines.

TitleProtein alterations associated with temozolomide resistance in subclones of human glioblastoma cell lines.
Authors
Sun, SWong, TSZhang, XQPu, JKLee, NPDay, PJNg, GKLui, WMLeung, GK
KeywordsChemoresistance
Glioma
Proteomics
Temozolomide
Two-dimensional gel electrophoresis
Issue Date2012
PublisherSpringer Netherlands
Citation
Journal Of Neuro-Oncology, 2012, v. 107 n. 1, p. 89-100 How to Cite?
DOI: http://dx.doi.org/10.1007/s11060-011-0729-8
AbstractTemozolomide (TMZ) is the standard chemotherapeutic agent for human malignant glioma, but intrinsic or acquired chemoresistance represents a major obstacle to successful treatment of this highly lethal group of tumours. Obtaining better understanding of the molecular mechanisms underlying TMZ resistance in malignant glioma is important for the development of better treatment strategies. We have successfully established a passage control line (D54-C10) and resistant variants (D54-P5 and D54-P10) from the parental TMZ-sensitive malignant glioma cell line D54-C0. The resistant sub-cell lines showed alterations in cell morphology, enhanced cell adhesion, increased migration capacities, and cell cycle arrests. Proteomic analysis identified a set of proteins that showed gradual changes in expression according to their 50% inhibitory concentration (IC(50)). Successful validation was provided by transcript profiling in another malignant glioma cell line U87-MG and its resistant counterparts. Moreover, three of the identified proteins (vimentin, cathepsin D and prolyl 4-hydroxylase, beta polypeptide) were confirmed to be upregulated in high-grade glioma. Our data suggest that acquired TMZ resistance in human malignant glioma is associated with promotion of malignant phenotypes, and our reported molecular candidates may serve not only as markers of chemoresistance but also as potential therapeutic targets in the treatment of TMZ-resistant human malignant glioma, providing a platform for future investigations.
Persistent Identifierhttp://hdl.handle.net/10722/144940
ISSN
1573-7373
2023 Impact Factor: 3.2
2023 SCImago Journal Rankings: 1.131
PubMed Central ID
PMC3273683
ISI Accession Number ID
WOS:000300313100010
Funding AgencyGrant Number
University of Hong Kong201007176020
Funding Information:

We would like to express our sincere gratitude for the insightful advice and support of Dr. Ching Fai Fung. The work was supported by a small project grant from the University of Hong Kong (project code 201007176020).

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Grants
Identification of therapeutic targets to combat glioblastoma drug resistance by proteomic profiling

 

DC FieldValueLanguage
dc.contributor.authorSun, Sen_HK
dc.contributor.authorWong, TSen_HK
dc.contributor.authorZhang, XQen_HK
dc.contributor.authorPu, JKen_HK
dc.contributor.authorLee, NPen_HK
dc.contributor.authorDay, PJen_HK
dc.contributor.authorNg, GKen_HK
dc.contributor.authorLui, WMen_HK
dc.contributor.authorLeung, GKen_HK
dc.date.accessioned2012-02-21T05:43:33Z-
dc.date.available2012-02-21T05:43:33Z-
dc.date.issued2012en_HK
dc.identifier.citationJournal Of Neuro-Oncology, 2012, v. 107 n. 1, p. 89-100en_HK
dc.identifier.issn1573-7373en_HK
dc.identifier.urihttp://hdl.handle.net/10722/144940-
dc.description.abstractTemozolomide (TMZ) is the standard chemotherapeutic agent for human malignant glioma, but intrinsic or acquired chemoresistance represents a major obstacle to successful treatment of this highly lethal group of tumours. Obtaining better understanding of the molecular mechanisms underlying TMZ resistance in malignant glioma is important for the development of better treatment strategies. We have successfully established a passage control line (D54-C10) and resistant variants (D54-P5 and D54-P10) from the parental TMZ-sensitive malignant glioma cell line D54-C0. The resistant sub-cell lines showed alterations in cell morphology, enhanced cell adhesion, increased migration capacities, and cell cycle arrests. Proteomic analysis identified a set of proteins that showed gradual changes in expression according to their 50% inhibitory concentration (IC(50)). Successful validation was provided by transcript profiling in another malignant glioma cell line U87-MG and its resistant counterparts. Moreover, three of the identified proteins (vimentin, cathepsin D and prolyl 4-hydroxylase, beta polypeptide) were confirmed to be upregulated in high-grade glioma. Our data suggest that acquired TMZ resistance in human malignant glioma is associated with promotion of malignant phenotypes, and our reported molecular candidates may serve not only as markers of chemoresistance but also as potential therapeutic targets in the treatment of TMZ-resistant human malignant glioma, providing a platform for future investigations.en_HK
dc.languageengen_US
dc.publisherSpringer Netherlandsen_US
dc.relation.ispartofJournal of Neuro-Oncologyen_HK
dc.rightsThe Author(s)en_US
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.en_US
dc.subjectChemoresistanceen_HK
dc.subjectGliomaen_HK
dc.subjectProteomicsen_HK
dc.subjectTemozolomideen_HK
dc.subjectTwo-dimensional gel electrophoresisen_HK
dc.titleProtein alterations associated with temozolomide resistance in subclones of human glioblastoma cell lines.en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4551/resserv?sid=springerlink&genre=article&atitle=Protein alterations associated with temozolomide resistance in subclones of human glioblastoma cell lines&title=Journal of Neuro-Oncology&issn=0167594X&date=2012-03-01&volume=107&issue=1& spage=89&authors=Stella Sun, T. S. Wong, X. Q. Zhang, <i>et al.</i>en_US
dc.identifier.emailWong, TS: thiansze@graduate.hku.hken_HK
dc.identifier.emailLee, NP: nikkilee@hku.hken_HK
dc.identifier.authorityWong, TS=rp00478en_HK
dc.identifier.authorityLee, NP=rp00263en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1007/s11060-011-0729-8en_HK
dc.identifier.pmid21979894en_HK
dc.identifier.pmcidPMC3273683-
dc.identifier.scopuseid_2-s2.0-84861697239en_HK
dc.identifier.hkuros206154-
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dc.identifier.volume107en_HK
dc.identifier.issue1en_HK
dc.identifier.spage89en_HK
dc.identifier.epage100en_HK
dc.identifier.eissn1573-7373en_US
dc.identifier.isiWOS:000300313100010-
dc.description.otherSpringer Open Choice, 21 Feb 2012en_US
dc.relation.projectIdentification of therapeutic targets to combat glioblastoma drug resistance by proteomic profiling-
dc.identifier.scopusauthoridSun, S=21740136100en_HK
dc.identifier.scopusauthoridWong, TS=7403531328en_HK
dc.identifier.scopusauthoridZhang, XQ=52264807800en_HK
dc.identifier.scopusauthoridPu, JK=35094475800en_HK
dc.identifier.scopusauthoridLee, NP=7402722690en_HK
dc.identifier.scopusauthoridDay, PJ=55234871600en_HK
dc.identifier.scopusauthoridNg, GK=55235756300en_HK
dc.identifier.scopusauthoridLui, WM=7101851125en_HK
dc.identifier.scopusauthoridLeung, GK=55235862400en_HK
dc.identifier.citeulike9884995-
dc.identifier.issnl0167-594X-

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