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Article: Suppression of lung tumor growth and metastasis in mice by adeno-associated virus-mediated expression of vasostatin

TitleSuppression of lung tumor growth and metastasis in mice by adeno-associated virus-mediated expression of vasostatin
Authors
Issue Date2008
PublisherAmerican Association for Cancer Research
Citation
Clinical Cancer Research, 2008, v. 14 n. 3, p. 939-949 How to Cite?
AbstractPurpose: Angiogenesis inhibitors have strong therapeutic potential as antitumor agents in suppressing tumor growth and metastatic progression. Vasostatin, the N-terminal domain of calreticulin, is a potent angiogenesis inhibitor. In this study, we determined the effectiveness of vasostatin delivered by recombinant pseudotype adeno-associated virus 2/5 (rAAV2/5-VAS) as a gene therapy approach for lung cancer treatment. Experimental Design: We used rAAV2/5 to deliver vasostatin intratumorally or systemically in different mouse lung tumor models - subcutaneous, orthotopic xenograft, and spontaneous metastasis lung tumor models. The therapeutic efficacy of rAAV2/5-VAS was determined by monitoring tumor volume, survival rate, and degree of neovascularization after treatment in these models. Results: Mice bearing subcutaneous tumor of rAAV2/5-VAS pretreated Lewis lung carcinoma cells showed <50% reduction in primary tumor volume and reduced spontaneous pulmonary metastases. The tumor-suppressive action of rAAV2/5-VAS in subcutaneous human lung tumor A549 xenograft correlated with a reduced number of capillary vessels in tumors. In the orthotopic xenograft model, rAAV2/5-VAS suppressed metastasis of A549 tumors to mediastinal lymph nodes and contralateral lung. Furthermore, treatment of immunocompetent mice in the spontaneous lung metastases model with rAAV2/5-VAS after primary tumor excision prolonged their median survival from 21 to 51.5 days. Conclusion: Our results show the effectiveness of rAAV2/5-VAS as an angiogenesis inhibitor in suppressing tumor growth during different stages of tumor progression, validating the application of rAAV2/5-VAS gene therapy in treatment against lung cancer. © 2008 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/68317
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKe, XCen_HK
dc.contributor.authorLai, YTen_HK
dc.contributor.authorLeung, Cen_HK
dc.contributor.authorTam, PKHen_HK
dc.contributor.authorXu, Ren_HK
dc.contributor.authorMai, HSen_HK
dc.date.accessioned2010-09-06T06:03:26Z-
dc.date.available2010-09-06T06:03:26Z-
dc.date.issued2008en_HK
dc.identifier.citationClinical Cancer Research, 2008, v. 14 n. 3, p. 939-949en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68317-
dc.description.abstractPurpose: Angiogenesis inhibitors have strong therapeutic potential as antitumor agents in suppressing tumor growth and metastatic progression. Vasostatin, the N-terminal domain of calreticulin, is a potent angiogenesis inhibitor. In this study, we determined the effectiveness of vasostatin delivered by recombinant pseudotype adeno-associated virus 2/5 (rAAV2/5-VAS) as a gene therapy approach for lung cancer treatment. Experimental Design: We used rAAV2/5 to deliver vasostatin intratumorally or systemically in different mouse lung tumor models - subcutaneous, orthotopic xenograft, and spontaneous metastasis lung tumor models. The therapeutic efficacy of rAAV2/5-VAS was determined by monitoring tumor volume, survival rate, and degree of neovascularization after treatment in these models. Results: Mice bearing subcutaneous tumor of rAAV2/5-VAS pretreated Lewis lung carcinoma cells showed <50% reduction in primary tumor volume and reduced spontaneous pulmonary metastases. The tumor-suppressive action of rAAV2/5-VAS in subcutaneous human lung tumor A549 xenograft correlated with a reduced number of capillary vessels in tumors. In the orthotopic xenograft model, rAAV2/5-VAS suppressed metastasis of A549 tumors to mediastinal lymph nodes and contralateral lung. Furthermore, treatment of immunocompetent mice in the spontaneous lung metastases model with rAAV2/5-VAS after primary tumor excision prolonged their median survival from 21 to 51.5 days. Conclusion: Our results show the effectiveness of rAAV2/5-VAS as an angiogenesis inhibitor in suppressing tumor growth during different stages of tumor progression, validating the application of rAAV2/5-VAS gene therapy in treatment against lung cancer. © 2008 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Researchen_US
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshAdenocarcinoma - pathologyen_HK
dc.subject.meshAngiogenesis Inhibitors - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCalreticulin - genetics - pharmacologyen_HK
dc.subject.meshCell Division - drug effectsen_HK
dc.subject.meshCloning, Molecularen_HK
dc.subject.meshDependovirus - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLung Neoplasms - pathologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshNeoplasm Metastasis - prevention & controlen_HK
dc.subject.meshPeptide Fragments - genetics - pharmacologyen_HK
dc.subject.meshRecombinant Proteins - pharmacologyen_HK
dc.titleSuppression of lung tumor growth and metastasis in mice by adeno-associated virus-mediated expression of vasostatinen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=14&issue=3&spage=939&epage=949&date=2008&atitle=Suppression+of+lung+tumor+growth+and+metastasis+in+mice+by+adeno-associated+virus-mediated+expression+of+vasostatinen_HK
dc.identifier.emailTam, PKH:paultam@hkucc.hku.hken_HK
dc.identifier.emailMai, HS:mhsham@hkucc.hku.hken_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.identifier.authorityMai, HS=rp00380en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1158/1078-0432.CCR-07-1930en_HK
dc.identifier.pmid18245558-
dc.identifier.scopuseid_2-s2.0-39049165759en_HK
dc.identifier.hkuros140955en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-39049165759&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issue3en_HK
dc.identifier.spage939en_HK
dc.identifier.epage949en_HK
dc.identifier.eissn1557-3265-
dc.identifier.isiWOS:000252882400042-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridKe, XC=35083699100en_HK
dc.identifier.scopusauthoridLai, YT=35083771600en_HK
dc.identifier.scopusauthoridLeung, C=35083863700en_HK
dc.identifier.scopusauthoridTam, PKH=7202539421en_HK
dc.identifier.scopusauthoridXu, R=7402813857en_HK
dc.identifier.scopusauthoridMai, HS=7003729109en_HK

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