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Article: ITGAV targeting as a therapeutic approach for treatment of metastatic breast cancer

TitleITGAV targeting as a therapeutic approach for treatment of metastatic breast cancer
Authors
KeywordsITGAV
breast cancer
cilengitide
metastasis
Issue Date2020
PublisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajcr.us
Citation
American Journal of Cancer Research, 2020, v. 10 n. 1, p. 211-223 How to Cite?
AbstractDuring tumorigenesis and metastasis, integrins regulate localization and activity of proteolytic enzymes that remodel the extracellular matrix. Previous studies have demonstrated blocking of αVβ3 to effectively inhibit proliferation, angiogenesis, and the survival of various cancer cell types. However, little is known about the functional role of the integrin subunit alpha-V gene (ITGAV) in metastatic breast cancer. In this study, ITGAV knockdown was used to identify the molecular mechanism by which ITGAV promotes tumorigenesis, metastasis, proliferation, invasion, and cellular self-renewal. The effectiveness of an ITGAV antagonist, cilengitide, for breast cancer treatment was investigated in vivo. Analysis of publicly available data demonstrated that overexpression of ITGAV was associated with poor relapse free survival of breast cancer patients. Silencing of ITGAV inhibited cell proliferation, invasion, and self-renewal of breast cancer cell lines by altering expression of BCL2 and PXN. The use of cilengitide significantly reduced lung metastasis in a metastatic breast cancer animal model. In conclusion, overexpression of ITGAV contributes to breast cancer metastasis through upregulation of PXN. Targeting ITGAV is a potential treatment for metastatic breast cancer as well as primary breast tumors with high ITGAV expression. ITGAV expression levels may be useful predictors of patient treatment and outcome responses.
Persistent Identifierhttp://hdl.handle.net/10722/280984
ISSN
2019 Impact Factor: 5.177
2015 SCImago Journal Rankings: 3.756
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCheuk, IWY-
dc.contributor.authorSiu, MT-
dc.contributor.authorHO, JCW-
dc.contributor.authorChen, J-
dc.contributor.authorShin, VY-
dc.contributor.authorKwong, A-
dc.date.accessioned2020-02-25T07:43:36Z-
dc.date.available2020-02-25T07:43:36Z-
dc.date.issued2020-
dc.identifier.citationAmerican Journal of Cancer Research, 2020, v. 10 n. 1, p. 211-223-
dc.identifier.issn2156-6976-
dc.identifier.urihttp://hdl.handle.net/10722/280984-
dc.description.abstractDuring tumorigenesis and metastasis, integrins regulate localization and activity of proteolytic enzymes that remodel the extracellular matrix. Previous studies have demonstrated blocking of αVβ3 to effectively inhibit proliferation, angiogenesis, and the survival of various cancer cell types. However, little is known about the functional role of the integrin subunit alpha-V gene (ITGAV) in metastatic breast cancer. In this study, ITGAV knockdown was used to identify the molecular mechanism by which ITGAV promotes tumorigenesis, metastasis, proliferation, invasion, and cellular self-renewal. The effectiveness of an ITGAV antagonist, cilengitide, for breast cancer treatment was investigated in vivo. Analysis of publicly available data demonstrated that overexpression of ITGAV was associated with poor relapse free survival of breast cancer patients. Silencing of ITGAV inhibited cell proliferation, invasion, and self-renewal of breast cancer cell lines by altering expression of BCL2 and PXN. The use of cilengitide significantly reduced lung metastasis in a metastatic breast cancer animal model. In conclusion, overexpression of ITGAV contributes to breast cancer metastasis through upregulation of PXN. Targeting ITGAV is a potential treatment for metastatic breast cancer as well as primary breast tumors with high ITGAV expression. ITGAV expression levels may be useful predictors of patient treatment and outcome responses.-
dc.languageeng-
dc.publisherE-Century Publishing Corporation. The Journal's web site is located at http://www.ajcr.us-
dc.relation.ispartofAmerican Journal of Cancer Research-
dc.subjectITGAV-
dc.subjectbreast cancer-
dc.subjectcilengitide-
dc.subjectmetastasis-
dc.titleITGAV targeting as a therapeutic approach for treatment of metastatic breast cancer-
dc.typeArticle-
dc.identifier.emailCheuk, IWY: isacheuk@hku.hk-
dc.identifier.emailSiu, MT: jensiu@hku.hk-
dc.identifier.emailChen, J: gary0526@hku.hk-
dc.identifier.emailShin, VY: vyshin@hku.hk-
dc.identifier.emailKwong, A: avakwong@hku.hk-
dc.identifier.authorityShin, VY=rp02000-
dc.identifier.authorityKwong, A=rp01734-
dc.description.naturepublished_or_final_version-
dc.identifier.pmid32064162-
dc.identifier.pmcidPMC7017729-
dc.identifier.hkuros309183-
dc.identifier.volume10-
dc.identifier.issue1-
dc.identifier.spage211-
dc.identifier.epage223-
dc.identifier.isiWOS:000508940800013-
dc.publisher.placeUnited States-

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