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Conference Paper: Identifying molecular candidates associated with acquired temozolomide resistance in human malignant glioma - a proteomics approach
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TitleIdentifying molecular candidates associated with acquired temozolomide resistance in human malignant glioma - a proteomics approach
 
AuthorsLeung, GKK
Sun, S
Wong, STS
Zhang, X
Pu, JKS
Lui, WM
 
Issue Date2011
 
PublisherEANS 2011.
 
CitationThe 14th European Congress of Neurosurgery (EANS 2011), Rome, Italy, 9-14 October 2011. [How to Cite?]
 
AbstractTemozolomide (TMZ) provides significant benefits in the treatment of malignant glioma but many patients continue to suffer from progressive or recurrent diseases due to their tumours’ intrinsic or acquired resistance to TMZ. Understanding the molecular mechanism underlying TMZ-resistance is important for the development of novel treatment strategies. OBJECTIVES: To employ proteomic profiling to study the global protein expression changes in TMZ-resistant malignant glioma cell-lines, and to investigate the potential role of one of the identified protein candidates, prolyl 4-hydroxylase, beta polypeptide (P4HB). MATERIALS AND METHOD: Human malignant glioma cell-lines (D54 and U87) with acquired TMZ-resistance were developed, and protein profiling analysis was performed using two dimensional gel electrophoresis (2DE). Potential protein spot candidates were identified by MALDI-TOF/TOF. Transient transfection with small interfering RNAs was used to knock down potential candidates to study their biological roles. RESULTS: Fifteen spots were identified as the most dysregulated proteins in TMZ-resistant glioma cells. Amongst these, the protein P4HB was found to be consistently dysregulated in D54 and U87. Transient knock-down was found to significantly down-regulate P4HB expression and increase TMZ-induced apoptosis. CONCLUSION: P4HB plays an important role in hypoxia-induced cell death. The present study describes its role in the regulation of apoptosis in TMZ-treated malignant glioma cells. P4HB is a potential candidate for future studies in TMZ-induced cytotoxicity and novel therapeutic strategies for the treatment of TMZ-resistant malignant glioma.
 
DC FieldValue
dc.contributor.authorLeung, GKK
 
dc.contributor.authorSun, S
 
dc.contributor.authorWong, STS
 
dc.contributor.authorZhang, X
 
dc.contributor.authorPu, JKS
 
dc.contributor.authorLui, WM
 
dc.date.accessioned2012-08-16T06:11:08Z
 
dc.date.available2012-08-16T06:11:08Z
 
dc.date.issued2011
 
dc.description.abstractTemozolomide (TMZ) provides significant benefits in the treatment of malignant glioma but many patients continue to suffer from progressive or recurrent diseases due to their tumours’ intrinsic or acquired resistance to TMZ. Understanding the molecular mechanism underlying TMZ-resistance is important for the development of novel treatment strategies. OBJECTIVES: To employ proteomic profiling to study the global protein expression changes in TMZ-resistant malignant glioma cell-lines, and to investigate the potential role of one of the identified protein candidates, prolyl 4-hydroxylase, beta polypeptide (P4HB). MATERIALS AND METHOD: Human malignant glioma cell-lines (D54 and U87) with acquired TMZ-resistance were developed, and protein profiling analysis was performed using two dimensional gel electrophoresis (2DE). Potential protein spot candidates were identified by MALDI-TOF/TOF. Transient transfection with small interfering RNAs was used to knock down potential candidates to study their biological roles. RESULTS: Fifteen spots were identified as the most dysregulated proteins in TMZ-resistant glioma cells. Amongst these, the protein P4HB was found to be consistently dysregulated in D54 and U87. Transient knock-down was found to significantly down-regulate P4HB expression and increase TMZ-induced apoptosis. CONCLUSION: P4HB plays an important role in hypoxia-induced cell death. The present study describes its role in the regulation of apoptosis in TMZ-treated malignant glioma cells. P4HB is a potential candidate for future studies in TMZ-induced cytotoxicity and novel therapeutic strategies for the treatment of TMZ-resistant malignant glioma.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationThe 14th European Congress of Neurosurgery (EANS 2011), Rome, Italy, 9-14 October 2011. [How to Cite?]
 
dc.identifier.hkuros204735
 
dc.identifier.urihttp://hdl.handle.net/10722/160435
 
dc.languageeng
 
dc.publisherEANS 2011.
 
dc.publisher.placeItaly
 
dc.relation.ispartof14th European Congress of Neurosurgery, EANS 2011
 
dc.titleIdentifying molecular candidates associated with acquired temozolomide resistance in human malignant glioma - a proteomics approach
 
dc.typeConference_Paper
 
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<item><contributor.author>Leung, GKK</contributor.author>
<contributor.author>Sun, S</contributor.author>
<contributor.author>Wong, STS</contributor.author>
<contributor.author>Zhang, X</contributor.author>
<contributor.author>Pu, JKS</contributor.author>
<contributor.author>Lui, WM</contributor.author>
<date.accessioned>2012-08-16T06:11:08Z</date.accessioned>
<date.available>2012-08-16T06:11:08Z</date.available>
<date.issued>2011</date.issued>
<identifier.citation>The 14th European Congress of Neurosurgery (EANS 2011), Rome, Italy, 9-14 October 2011.</identifier.citation>
<identifier.uri>http://hdl.handle.net/10722/160435</identifier.uri>
<description.abstract>Temozolomide (TMZ) provides significant benefits in the treatment of malignant glioma but many patients continue to suffer from progressive or recurrent diseases due to their tumours&#8217; intrinsic or acquired resistance to TMZ. Understanding the molecular mechanism underlying TMZ-resistance is important for the development of novel treatment strategies. OBJECTIVES: To employ proteomic profiling to study the global protein expression changes in TMZ-resistant malignant glioma cell-lines, and to investigate the potential role of one of the identified protein candidates, prolyl 4-hydroxylase, beta polypeptide (P4HB). MATERIALS AND METHOD: Human malignant glioma cell-lines (D54 and U87) with acquired TMZ-resistance were developed, and protein profiling analysis was performed using two dimensional gel electrophoresis (2DE). Potential protein spot candidates were identified by MALDI-TOF/TOF. Transient transfection with small interfering RNAs was used to knock down potential candidates to study their biological roles. RESULTS: Fifteen spots were identified as the most dysregulated proteins in TMZ-resistant glioma cells. Amongst these, the protein P4HB was found to be consistently dysregulated in D54 and U87. Transient knock-down was found to significantly down-regulate P4HB expression and increase TMZ-induced apoptosis. CONCLUSION: P4HB plays an important role in hypoxia-induced cell death. The present study describes its role in the regulation of apoptosis in TMZ-treated malignant glioma cells. P4HB is a potential candidate for future studies in TMZ-induced cytotoxicity and novel therapeutic strategies for the treatment of TMZ-resistant malignant glioma.</description.abstract>
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