File Download
Supplementary

Conference Paper: Identifying molecular candidates associated with acquired temozolomide resistance in human malignant glioma - a proteomics approach

TitleIdentifying molecular candidates associated with acquired temozolomide resistance in human malignant glioma - a proteomics approach
Authors
Issue Date2011
PublisherEANS 2011.
Citation
The 14th European Congress of Neurosurgery (EANS 2011), Rome, Italy, 9-14 October 2011. How to Cite?
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’ 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.
Persistent Identifierhttp://hdl.handle.net/10722/160435

 

DC FieldValueLanguage
dc.contributor.authorLeung, GKKen_US
dc.contributor.authorSun, Sen_US
dc.contributor.authorWong, STSen_US
dc.contributor.authorZhang, Xen_US
dc.contributor.authorPu, JKSen_US
dc.contributor.authorLui, WMen_US
dc.date.accessioned2012-08-16T06:11:08Z-
dc.date.available2012-08-16T06:11:08Z-
dc.date.issued2011en_US
dc.identifier.citationThe 14th European Congress of Neurosurgery (EANS 2011), Rome, Italy, 9-14 October 2011.en_US
dc.identifier.urihttp://hdl.handle.net/10722/160435-
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.languageengen_US
dc.publisherEANS 2011.-
dc.relation.ispartof14th European Congress of Neurosurgery, EANS 2011en_US
dc.titleIdentifying molecular candidates associated with acquired temozolomide resistance in human malignant glioma - a proteomics approachen_US
dc.typeConference_Paperen_US
dc.identifier.emailLeung, GKK: gkkleung@hku.hken_US
dc.identifier.emailSun, S: ssun@hku.hken_US
dc.identifier.emailWong, STS: wongtsa@hkucc.hku.hken_US
dc.identifier.emailZhang, X: xqzhang6@hku.hken_US
dc.identifier.emailLui, WM: mattlui@hku.hk-
dc.identifier.authorityLeung, GKK=rp00522en_US
dc.identifier.authorityWong, STS=rp00478en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros204735en_US
dc.publisher.placeItaly-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats