Tamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissues
Autor(a) principal: | |
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Data de Publicação: | 1997 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNIFESP |
Texto Completo: | http://repositorio.unifesp.br/11600/43247 http://cancerres.aacrjournals.org/content/57/3/378 |
Resumo: | Tamoxifen (TAM) exerts a long-term suppressive effect on human breast cancer cell proliferation on. To determine whether the effects of TAM are mediated by specific gene activation or repression, normal and tumoral human breast tissues obtained before and during TAM treatment were analysed by differential display technique, Total RNA for differential display analysis was obtained from breast tissues from two women with the diagnosis of estrogen receptor-positive stage II (T(2)N(1)M(0)) infiltrating ductal carcinoma, made by incisional biopsy, followed by modified radical mastectomy performed after a 30-day treatment with TAM (20 mg/day), One 202-bp cDNA band, AP5-1, was present in normal and tumoral biopsy samples, but was absent in breast tissue obtained during TAM treatment, and was confirmed by Northern hybridization, which showed a 2.7-kb band in both patients, The differentially expressed cDNA fragment showed 99% homology to Homo sapiens CD36 gene, a glycoprotein that acts as a receptor for the extracellular matrix proteins thrombospondin-1, collagen types I and IV, and oxidized low-density lipoprotein, These results indicate that the down-regulation of CD36 induced by TAM might represent alternative or additional mechanisms of action of this drug affecting the functions of thrombospondin-1, which is involved in hematogenous tumor spread, invasion and angiogenesis, and oxidized low-density lipoprotein, playing a role in inhibition of arteriosclerosis. The multiple functions affected by the down-regulation of CD36 by TAM warrant the need for additional studies. |
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Repositório Institucional da UNIFESP |
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Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP]Salicioni, Ana M.Russo, I. H.Higgy, N. A.Gebrim, Luiz H [UNIFESP]Russo, J.FOX CHASE CANC CTRUniversidade Federal de São Paulo (UNIFESP)2018-06-15T16:39:14Z2018-06-15T16:39:14Z1997-02-01Cancer Research. Philadelphia: Amer Assoc Cancer Research, v. 57, n. 3, p. 378-381, 1997.0008-5472http://repositorio.unifesp.br/11600/43247http://cancerres.aacrjournals.org/content/57/3/378WOS:A1997WF51700008Tamoxifen (TAM) exerts a long-term suppressive effect on human breast cancer cell proliferation on. To determine whether the effects of TAM are mediated by specific gene activation or repression, normal and tumoral human breast tissues obtained before and during TAM treatment were analysed by differential display technique, Total RNA for differential display analysis was obtained from breast tissues from two women with the diagnosis of estrogen receptor-positive stage II (T(2)N(1)M(0)) infiltrating ductal carcinoma, made by incisional biopsy, followed by modified radical mastectomy performed after a 30-day treatment with TAM (20 mg/day), One 202-bp cDNA band, AP5-1, was present in normal and tumoral biopsy samples, but was absent in breast tissue obtained during TAM treatment, and was confirmed by Northern hybridization, which showed a 2.7-kb band in both patients, The differentially expressed cDNA fragment showed 99% homology to Homo sapiens CD36 gene, a glycoprotein that acts as a receptor for the extracellular matrix proteins thrombospondin-1, collagen types I and IV, and oxidized low-density lipoprotein, These results indicate that the down-regulation of CD36 induced by TAM might represent alternative or additional mechanisms of action of this drug affecting the functions of thrombospondin-1, which is involved in hematogenous tumor spread, invasion and angiogenesis, and oxidized low-density lipoprotein, playing a role in inhibition of arteriosclerosis. The multiple functions affected by the down-regulation of CD36 by TAM warrant the need for additional studies.FOX CHASE CANC CTR,BREAST CANC RES LAB,PHILADELPHIA,PA 19111UNIV FED SAO PAULO,ESCOLA PAULISTA MED,DEPT GYNECOL,MASTROL GRP,SAO PAULO,BRAZILUNIV FED SAO PAULO,ESCOLA PAULISTA MED,DEPT GYNECOL,MASTROL GRP,SAO PAULO,BRAZILWeb of Science378-381engAmer Assoc Cancer ResearchCancer ResearchTamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissuesinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/432472021-10-05 15:45:12.597metadata only accessoai:repositorio.unifesp.br:11600/43247Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652021-10-05T18:45:12Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false |
dc.title.en.fl_str_mv |
Tamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissues |
title |
Tamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissues |
spellingShingle |
Tamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissues Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP] |
title_short |
Tamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissues |
title_full |
Tamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissues |
title_fullStr |
Tamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissues |
title_full_unstemmed |
Tamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissues |
title_sort |
Tamoxifen down-regulates CD36 messenger RNA levels in normal and neoplastic human breast tissues |
author |
Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP] |
author_facet |
Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP] Salicioni, Ana M. Russo, I. H. Higgy, N. A. Gebrim, Luiz H [UNIFESP] Russo, J. |
author_role |
author |
author2 |
Salicioni, Ana M. Russo, I. H. Higgy, N. A. Gebrim, Luiz H [UNIFESP] Russo, J. |
author2_role |
author author author author author |
dc.contributor.institution.none.fl_str_mv |
FOX CHASE CANC CTR Universidade Federal de São Paulo (UNIFESP) |
dc.contributor.author.fl_str_mv |
Silva, Ismael Dale Cotrim Guerreiro da [UNIFESP] Salicioni, Ana M. Russo, I. H. Higgy, N. A. Gebrim, Luiz H [UNIFESP] Russo, J. |
description |
Tamoxifen (TAM) exerts a long-term suppressive effect on human breast cancer cell proliferation on. To determine whether the effects of TAM are mediated by specific gene activation or repression, normal and tumoral human breast tissues obtained before and during TAM treatment were analysed by differential display technique, Total RNA for differential display analysis was obtained from breast tissues from two women with the diagnosis of estrogen receptor-positive stage II (T(2)N(1)M(0)) infiltrating ductal carcinoma, made by incisional biopsy, followed by modified radical mastectomy performed after a 30-day treatment with TAM (20 mg/day), One 202-bp cDNA band, AP5-1, was present in normal and tumoral biopsy samples, but was absent in breast tissue obtained during TAM treatment, and was confirmed by Northern hybridization, which showed a 2.7-kb band in both patients, The differentially expressed cDNA fragment showed 99% homology to Homo sapiens CD36 gene, a glycoprotein that acts as a receptor for the extracellular matrix proteins thrombospondin-1, collagen types I and IV, and oxidized low-density lipoprotein, These results indicate that the down-regulation of CD36 induced by TAM might represent alternative or additional mechanisms of action of this drug affecting the functions of thrombospondin-1, which is involved in hematogenous tumor spread, invasion and angiogenesis, and oxidized low-density lipoprotein, playing a role in inhibition of arteriosclerosis. The multiple functions affected by the down-regulation of CD36 by TAM warrant the need for additional studies. |
publishDate |
1997 |
dc.date.issued.fl_str_mv |
1997-02-01 |
dc.date.accessioned.fl_str_mv |
2018-06-15T16:39:14Z |
dc.date.available.fl_str_mv |
2018-06-15T16:39:14Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.citation.fl_str_mv |
Cancer Research. Philadelphia: Amer Assoc Cancer Research, v. 57, n. 3, p. 378-381, 1997. |
dc.identifier.uri.fl_str_mv |
http://repositorio.unifesp.br/11600/43247 http://cancerres.aacrjournals.org/content/57/3/378 |
dc.identifier.issn.none.fl_str_mv |
0008-5472 |
dc.identifier.wos.none.fl_str_mv |
WOS:A1997WF51700008 |
identifier_str_mv |
Cancer Research. Philadelphia: Amer Assoc Cancer Research, v. 57, n. 3, p. 378-381, 1997. 0008-5472 WOS:A1997WF51700008 |
url |
http://repositorio.unifesp.br/11600/43247 http://cancerres.aacrjournals.org/content/57/3/378 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.ispartof.none.fl_str_mv |
Cancer Research |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
378-381 |
dc.publisher.none.fl_str_mv |
Amer Assoc Cancer Research |
publisher.none.fl_str_mv |
Amer Assoc Cancer Research |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UNIFESP instname:Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
instname_str |
Universidade Federal de São Paulo (UNIFESP) |
instacron_str |
UNIFESP |
institution |
UNIFESP |
reponame_str |
Repositório Institucional da UNIFESP |
collection |
Repositório Institucional da UNIFESP |
repository.name.fl_str_mv |
Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP) |
repository.mail.fl_str_mv |
|
_version_ |
1802764115875201024 |