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Article: Beyond antiangiogenesis: Intratumorally injected bevacizumab plays a cisplatin-sensitizing role in squamous cell carcinomas in mice

TitleBeyond antiangiogenesis: Intratumorally injected bevacizumab plays a cisplatin-sensitizing role in squamous cell carcinomas in mice
Authors
KeywordsAntiangiogenesis
Anticancer mechanism
Bevacizumab
Cisplatin
Squamous cell carcinoma
Issue Date2011
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/CHE
Citation
Chemotherapy, 2011, v. 57 n. 3, p. 244-252 How to Cite?
AbstractBackground: The anticancer mechanism of bevacizumab beyond antiangiogenesis remains unclear. Here, we investigated whether intratumorally injected bevacizumab could serve as an effective cisplatin sensitizer in squamous cell carcinoma (SCC) in vivo. Methods: Hela and SCC-VII experimental SCC models were established to investigate the anticancer effect of bevacizumab plus cisplatin and the underlying mechanism using immunostaining, TUNEL, and Western blot assays. Results: Bevacizumab-cisplatin therapy markedly inhibited tumor growth and significantly increased survival in both Hela- and SCC-VII-bearing mice compared with single-agent treatments and the untreated control, respectively. Immunostaining of CD34 showed that intratumorally injected bevacizumab significantly reduced microvessel density in bevacizumab-cisplatin and bevacizumab-alone groups of Hela xenografts. TUNEL assay showed that bevacizumab-cisplatin significantly promoted tumor cell apoptosis compared with single-agent treatments and untreated controls in these 2 models. Western blot showed that upregulation of cleaved caspase-3 and downregulation of Bcl-2 and p-Erk expressions are part of the molecular mechanisms beyond angiogenesis which contribute to the cooperative effect of bevacizumab plus cisplatin in the 2 SCC models. Conclusions: Bevacizumab functions not only as an angiogenesis inhibitor but also as a chemosensitizer which enhances the cytotoxicity of cisplatin and promotes apoptosis of SCC cells. Copyright © 2011 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/134990
ISSN
2023 Impact Factor: 2.0
2023 SCImago Journal Rankings: 0.663
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China39470754
National '985 Project' of China985-2-040-115
Funding Information:

We thank Dr. Nianhui Cui for providing the SCC-VII cell line for this study. This study was supported by the National Natural Science Foundation of China (39470754) and the National '985 Project' of China (985-2-040-115).

References

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorDong, Len_HK
dc.contributor.authorBi, Qen_HK
dc.contributor.authorGe, Xen_HK
dc.contributor.authorZhang, Xen_HK
dc.contributor.authorWu, Den_HK
dc.contributor.authorFu, Jen_HK
dc.contributor.authorZhang, Cen_HK
dc.contributor.authorWang, Cen_HK
dc.contributor.authorLi, Sen_HK
dc.date.accessioned2011-07-27T01:25:30Z-
dc.date.available2011-07-27T01:25:30Z-
dc.date.issued2011en_HK
dc.identifier.citationChemotherapy, 2011, v. 57 n. 3, p. 244-252en_HK
dc.identifier.issn0009-3157en_HK
dc.identifier.urihttp://hdl.handle.net/10722/134990-
dc.description.abstractBackground: The anticancer mechanism of bevacizumab beyond antiangiogenesis remains unclear. Here, we investigated whether intratumorally injected bevacizumab could serve as an effective cisplatin sensitizer in squamous cell carcinoma (SCC) in vivo. Methods: Hela and SCC-VII experimental SCC models were established to investigate the anticancer effect of bevacizumab plus cisplatin and the underlying mechanism using immunostaining, TUNEL, and Western blot assays. Results: Bevacizumab-cisplatin therapy markedly inhibited tumor growth and significantly increased survival in both Hela- and SCC-VII-bearing mice compared with single-agent treatments and the untreated control, respectively. Immunostaining of CD34 showed that intratumorally injected bevacizumab significantly reduced microvessel density in bevacizumab-cisplatin and bevacizumab-alone groups of Hela xenografts. TUNEL assay showed that bevacizumab-cisplatin significantly promoted tumor cell apoptosis compared with single-agent treatments and untreated controls in these 2 models. Western blot showed that upregulation of cleaved caspase-3 and downregulation of Bcl-2 and p-Erk expressions are part of the molecular mechanisms beyond angiogenesis which contribute to the cooperative effect of bevacizumab plus cisplatin in the 2 SCC models. Conclusions: Bevacizumab functions not only as an angiogenesis inhibitor but also as a chemosensitizer which enhances the cytotoxicity of cisplatin and promotes apoptosis of SCC cells. Copyright © 2011 S. Karger AG, Basel.en_HK
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/CHEen_HK
dc.relation.ispartofChemotherapyen_HK
dc.subjectAntiangiogenesis-
dc.subjectAnticancer mechanism-
dc.subjectBevacizumab-
dc.subjectCisplatin-
dc.subjectSquamous cell carcinoma-
dc.subject.meshAngiogenesis Inhibitors - therapeutic useen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAntibodies, Monoclonal - therapeutic useen_HK
dc.subject.meshAntibodies, Monoclonal, Humanizeden_HK
dc.subject.meshAntigens, CD34 - metabolismen_HK
dc.subject.meshAntineoplastic Combined Chemotherapy Protocols - therapeutic useen_HK
dc.subject.meshCarcinoma, Squamous Cell - drug therapy - mortality - pathologyen_HK
dc.subject.meshCaspase 3 - metabolismen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCisplatin - therapeutic useen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshExtracellular Signal-Regulated MAP Kinases - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshNeovascularization, Pathologicen_HK
dc.subject.meshProto-Oncogene Proteins c-bcl-2 - metabolismen_HK
dc.subject.meshSurvival Rateen_HK
dc.titleBeyond antiangiogenesis: Intratumorally injected bevacizumab plays a cisplatin-sensitizing role in squamous cell carcinomas in miceen_HK
dc.typeArticleen_HK
dc.identifier.emailZhang, C:zhangcf@hku.hken_HK
dc.identifier.authorityZhang, C=rp01408en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000326485en_HK
dc.identifier.pmid21597289-
dc.identifier.scopuseid_2-s2.0-79955960642en_HK
dc.identifier.hkuros188473en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79955960642&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume57en_HK
dc.identifier.issue3en_HK
dc.identifier.spage244en_HK
dc.identifier.epage252en_HK
dc.identifier.isiWOS:000291159500010-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridWang, Y=35847885800en_HK
dc.identifier.scopusauthoridDong, L=36445358100en_HK
dc.identifier.scopusauthoridBi, Q=36445153200en_HK
dc.identifier.scopusauthoridGe, X=12762412200en_HK
dc.identifier.scopusauthoridZhang, X=25642305200en_HK
dc.identifier.scopusauthoridWu, D=7404298374en_HK
dc.identifier.scopusauthoridFu, J=53879609400en_HK
dc.identifier.scopusauthoridZhang, C=7405494609en_HK
dc.identifier.scopusauthoridWang, C=35276383300en_HK
dc.identifier.scopusauthoridLi, S=8277634200en_HK
dc.identifier.issnl0009-3157-

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