Insulin-like growth factor-1 and 17 beta-estradiol down-regulate prostate apoptosis response-4 expression in MCF-7 breast cancer cells

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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 CASOLARI, Debora A.
PEREIRA, Michelly C. FMUSP-HC
GARCIA, Simone A. De Bessa FMUSP-HC
NAGAI, Maria A. FMUSP-HC
dc.date.issued 2011
dc.identifier.citation INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, v.28, n.3, p.337-342, 2011
dc.identifier.issn 1107-3756
dc.identifier.uri http://observatorio.fm.usp.br/handle/OPI/22884
dc.description.abstract The PKC apoptosis WTI regulator gene, also named prostate apoptosis response-4 (PAR-4), encodes a pro-apoptotic protein that sensitizes cells to numerous apoptotic stimuli. Insulin-like growth factor-1 (IGF-1) and 17 beta-estradiol (E2), two important factors for breast cancer development and progression, have been shown to down-regulate PAR-4 expression and inhibit apoptosis induced by PAR-4 in neuronal cells. In this study, we sought to investigate the mechanisms of regulation of PAR-4 gene expression in MCF-7 cells treated with E2 or IGF-1. E2 (10 nM) and IGF-1 (12.5 nM) each down-regulated PAR-4 expression in MCF-7 cells after 24 h of treatment. The effect of E2 was dependent on ER activation, as demonstrated by an increase in PAR-4 expression when cells were pretreated for 1 h with 1 mu M ICI-182,780 (ICI) before receiving E2 plus ICI. The effect of IGF-1 was abolished by pre-treatment for 1 h with 30 mu M LY294002 (a specific PI3-K inhibitor), and significantly inhibited by 30 mu M SB202190 (a specific p38MAPK inhibitor). We also demonstrated that E2 acts synergistically with IGF-1, resulting in greater down-regulation of PAR-4 mRNA expression compared with E2 or IGF-1 alone. Our results show for the first time that E2 and IGF-1 inhibit PAR-4 gene expression in MCF-7 cells, suggesting that this down-regulation may provide a selective advantage for breast cancer cell survival.
dc.description.sponsorship · FAPESP - Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [06/01026-0]
· CNPq (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico) [304949/2006-0]
dc.language.iso eng
dc.publisher SPANDIDOS PUBL LTD
dc.relation.ispartof International Journal of Molecular Medicine
dc.rights restrictedAccess
dc.subject breast cancer; estrogen; estrogen receptor; prostate apoptosis response-4; insulin-like growth factor-1
dc.subject.other decreased expression; protein par-4; phosphorylation; activation; pathway; alpha; statistics; target
dc.title Insulin-like growth factor-1 and 17 beta-estradiol down-regulate prostate apoptosis response-4 expression in MCF-7 breast cancer cells
dc.type article
dc.rights.holder Copyright SPANDIDOS PUBL LTD
dc.description.group LIM/24
dc.identifier.doi 10.3892/ijmm.2011.691
dc.identifier.pmid 21567071
dc.type.category original article
dc.type.version publishedVersion
hcfmusp.author PEREIRA, Michelly C.:FM:
hcfmusp.author GARCIA, Simone A. De Bessa:FM:MDR
hcfmusp.author NAGAI, Maria A.:FM:MDR
hcfmusp.author.external · CASOLARI, Debora A.:Univ Sao Paulo, Disciplina Oncol, Dept Radiol, Fac Med, BR-01246903 Sao Paulo, Brazil
hcfmusp.origem.id WOS:000293603100006
hcfmusp.origem.id 2-s2.0-79960009788
hcfmusp.publisher.city ATHENS
hcfmusp.publisher.country GREECE
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dc.description.index MEDLINE
hcfmusp.citation.scopus 9
hcfmusp.affiliation.country Brasil
hcfmusp.scopus.lastupdate 2021-08-27


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