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DC Field | Value | Language |
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dc.contributor | Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP | - |
dc.contributor.author | PEREIRA, Michelly C. | - |
dc.contributor.author | BESSA-GARCIA, Simone A. De | - |
dc.contributor.author | BURIKHANOV, Ravshan | - |
dc.contributor.author | PAVANELLI, Ana Carolina | - |
dc.contributor.author | ANTUNES, Lourival | - |
dc.contributor.author | RANGNEKAR, Vivek M. | - |
dc.contributor.author | NAGAI, Maria A. | - |
dc.date.accessioned | 2013-09-23T16:37:33Z | - |
dc.date.available | 2013-09-23T16:37:33Z | - |
dc.date.issued | 2013 | - |
dc.identifier.citation | INTERNATIONAL JOURNAL OF ONCOLOGY, v.43, n.2, p.531-538, 2013 | - |
dc.identifier.issn | 1019-6439 | - |
dc.identifier.uri | https://observatorio.fm.usp.br/handle/OPI/1886 | - |
dc.description.abstract | Experimental evidence indicates that prostate apoptosis response-4 (Par-4, also known as PAWR) is a key regulator of cancer cell survival and may be a target for cancer-selective targeted therapeutics. Par-4 was first identified in prostate cancer cells undergoing apoptosis. Both intracellular and extracellular Par-4 have been implicated in apoptosis. Relatively little is known about the role of Par-4 in breast cancer cell apoptosis. In this study, we sought to investigate the effects of Par-4 expression on cell proliferation, apoptosis and drug sensitivity in breast cancer cells. MCF-7 cells were stably transfected with expression vectors for Par-4, or transiently transfected with siRNA for Par-4 knockdown. Cell proliferation assays were performed using MTT and apoptosis was evaluated using acridine orange staining, fluorescence microscopy and flow cytometry. Par-4 overexpression reduced MCF-7 proliferation rates. Conversely, Par-4 knockdown led to increased MCF-7 proliferation. Par-4 downregulation also led to increased BCL-2 and reduced BID expression. Par-4 overexpression did not affect the cell cycle profile. However, MCF-7 cells with increased Par-4 expression showed reduced ERK phosphorylation, suggesting that the inhibition of cell proliferation promoted by Par-4 may be mediated by the MAPK/ERK1/2 pathway. MCF-7 cells with increased Par-4 expression showed a marginal increase in early apoptotic cells. Importantly, we found that Par-4 expression modulates apoptosis in response to docetaxel in MCF7 breast cancer cells. Par-4 exerts growth inhibitory effects on breast cancer cells and chemosensitizes them to docetaxel. | - |
dc.description.sponsorship | FAPESP - Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [2010/16543-5] | - |
dc.description.sponsorship | CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico) [305408/2009-7] | - |
dc.language.iso | eng | - |
dc.publisher | SPANDIDOS PUBL LTD | - |
dc.relation.ispartof | International Journal of Oncology | - |
dc.rights | restrictedAccess | - |
dc.subject | Par-4 | - |
dc.subject | breast cancer | - |
dc.subject | proliferation | - |
dc.subject | survival | - |
dc.subject | apoptosis | - |
dc.subject | docetaxel | - |
dc.subject.other | tumor-suppressor par-4 | - |
dc.subject.other | down-regulation | - |
dc.subject.other | caspase activation | - |
dc.subject.other | protein par-4 | - |
dc.subject.other | expression | - |
dc.subject.other | bcl-2 | - |
dc.subject.other | kinase | - |
dc.subject.other | growth | - |
dc.subject.other | pathway | - |
dc.subject.other | death | - |
dc.title | Prostate apoptosis response-4 is involved in the apoptosis response to docetaxel in MCF-7 breast cancer cells | - |
dc.type | article | - |
dc.rights.holder | Copyright SPANDIDOS PUBL LTD | - |
dc.identifier.doi | 10.3892/ijo.2013.1983 | - |
dc.identifier.pmid | 23760770 | - |
dc.subject.wos | Oncology | - |
dc.type.category | original article | - |
dc.type.version | publishedVersion | - |
hcfmusp.author.external | BURIKHANOV, Ravshan:Univ Kentucky, Lucille P Markey Canc Ctr, Lexington, KY USA | - |
hcfmusp.author.external | RANGNEKAR, Vivek M.:Univ Kentucky, Lucille P Markey Canc Ctr, Lexington, KY USA | - |
hcfmusp.description.beginpage | 531 | - |
hcfmusp.description.endpage | 538 | - |
hcfmusp.description.issue | 2 | - |
hcfmusp.description.volume | 43 | - |
hcfmusp.origem | WOS | - |
hcfmusp.origem.id | WOS:000321937100020 | - |
hcfmusp.origem.id | 2-s2.0-84879654301 | - |
hcfmusp.publisher.city | ATHENS | - |
hcfmusp.publisher.country | GREECE | - |
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dc.description.index | MEDLINE | - |
hcfmusp.remissive.sponsorship | CNPq | - |
hcfmusp.remissive.sponsorship | FAPESP | - |
hcfmusp.citation.scopus | 19 | - |
hcfmusp.scopus.lastupdate | 2024-04-12 | - |
Appears in Collections: | Artigos e Materiais de Revistas Científicas - FM/MDR Artigos e Materiais de Revistas Científicas - LIM/24 Artigos e Materiais de Revistas Científicas - ODS/03 |
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