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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 | TRAPE, Adriana Priscila | - |
dc.contributor.author | KATAYAMA, Maria Lucia Hirata | - |
dc.contributor.author | ROELA, Rosimeire Aparecida | - |
dc.contributor.author | BRENTANI, Helena | - |
dc.contributor.author | RAVACCI, Graziela Rosa | - |
dc.contributor.author | LIMA, Leandro de Araujo | - |
dc.contributor.author | BRENTANI, Maria Mitzi | - |
dc.date.accessioned | 2013-07-30T15:18:57Z | - |
dc.date.available | 2013-07-30T15:18:57Z | - |
dc.date.issued | 2012 | - |
dc.identifier.citation | MOLECULAR CANCER THERAPEUTICS, v.11, n.2, p.464-474, 2012 | - |
dc.identifier.issn | 1535-7163 | - |
dc.identifier.uri | https://observatorio.fm.usp.br/handle/OPI/1093 | - |
dc.description.abstract | HER-2-positive breast cancers frequently sustain elevated AKT/mTOR signaling, which has been associated with resistance to doxorubicin treatment. Here, we investigated whether rapamycin, an mTOR inhibitor, increased the sensitivity to doxorubicin therapy in two HER-2-overexpressing cell lines: C5.2, which was derived from the parental HB4a by transfection with HER-2 and SKBR3, which exhibits HER-2 amplification. The epithelial mammary cell line HB4a was also analyzed. The combined treatment using 20 nmol/L of rapamycin and 30 nmol/L of doxorubicin arrested HB4a and C5.2 cells in S to G(2)-M, whereas SKBR3 cells showed an increase in the G(0)-G(1) phase. Rapamycin increased the sensitivity to doxorubicin in HER-2-overexpressing cells by approximately 2-fold, suggesting that the combination displayed a more effective antiproliferative action. Gene expression profiling showed that these results might reflect alterations in genes involved in canonical pathways related to purine metabolism, oxidative phosphorylation, protein ubiquitination, and mitochondrial dysfunction. A set of 122 genes modulated by the combined treatment and specifically related to HER-2 overexpression was determined by finding genes commonly regulated in both C5.2 and SKBR3 that were not affected in HB4a cells. Network analysis of this particular set showed a smaller subgroup of genes in which coexpression pattern in HB4a cells was disrupted in C5.2 and SKBR3. Altogether, our data showed a subset of genes that might be more robust than individual markers in predicting the response of HER-2-overexpressing breast cancers to doxorubicin and rapamycin combination. | - |
dc.description.sponsorship | FAPESP | - |
dc.description.sponsorship | CnPq | - |
dc.language.iso | eng | - |
dc.publisher | AMER ASSOC CANCER RESEARCH | - |
dc.relation.ispartof | Molecular Cancer Therapeutics | - |
dc.rights | restrictedAccess | - |
dc.subject.other | breast-cancer cells | - |
dc.subject.other | topoisomerase-ii-alpha | - |
dc.subject.other | mammalian target | - |
dc.subject.other | her2 status | - |
dc.subject.other | mtor | - |
dc.subject.other | chemotherapy | - |
dc.subject.other | sensitivity | - |
dc.subject.other | therapy | - |
dc.subject.other | inhibitor | - |
dc.subject.other | pharmacokinetics | - |
dc.title | Gene Expression Profile in Response to Doxorubicin-Rapamycin Combined Treatment of HER-2-Overexpressing Human Mammary Epithelial Cell Lines | - |
dc.type | article | - |
dc.rights.holder | Copyright AMER ASSOC CANCER RESEARCH | - |
dc.identifier.doi | 10.1158/1535-7163.MCT-11-0033 | - |
dc.identifier.pmid | 22084168 | - |
dc.subject.wos | Oncology | - |
dc.type.category | original article | - |
dc.type.version | publishedVersion | - |
hcfmusp.author.external | LIMA, Leandro de Araujo:Hosp AC Camargo Fund Antonio Prudente, CIPE, Lab Bioinformat & Bioestat, Sao Paulo, Brazil | - |
hcfmusp.description.beginpage | 464 | - |
hcfmusp.description.endpage | 474 | - |
hcfmusp.description.issue | 2 | - |
hcfmusp.description.volume | 11 | - |
hcfmusp.origem | WOS | - |
hcfmusp.origem.id | 2-s2.0-84856830942 | - |
hcfmusp.origem.id | WOS:000300415300020 | - |
hcfmusp.publisher.city | PHILADELPHIA | - |
hcfmusp.publisher.country | USA | - |
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dc.description.index | MEDLINE | - |
hcfmusp.remissive.sponsorship | CNPq | - |
hcfmusp.remissive.sponsorship | FAPESP | - |
hcfmusp.lim.ref | 2012 | - |
hcfmusp.citation.scopus | 5 | - |
hcfmusp.scopus.lastupdate | 2024-04-12 | - |
Appears in Collections: | Artigos e Materiais de Revistas Científicas - FM/MDR Artigos e Materiais de Revistas Científicas - FM/MPS Artigos e Materiais de Revistas Científicas - LIM/21 Artigos e Materiais de Revistas Científicas - LIM/24 Artigos e Materiais de Revistas Científicas - LIM/35 |
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