Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid

Detalhes bibliográficos
Autor(a) principal: Snitcovsky,I.
Data de Publicação: 2003
Outros Autores: Katayama,M.L.H., Folgueira,M.A.A.K., Brentani,M.M.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Brazilian Journal of Medical and Biological Research
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001200019
Resumo: The objective of the present study was to determine the effects of retinoic acid on the growth of the mouse mammary cells HC11 and HC11ras, which are a model for in vitro breast cancer progression. The expression of the two classes (RARs and RXRs) of retinoic acid receptor mRNAs was determined by Northern blot analysis. Receptor functional integrity was determined by testing whether RAR ß mRNA could be induced by retinoic acid. The effects of a 72-h exposure to 50 µM 13-cis retinoic acid on HC11 and HC11ras cell proliferation and HC11 cell differentiation were investigated by flow cytometric cell cycle analysis, and by determination of ß-casein mRNA expression, respectively. The possibility that retinoic acid would induce the expression of the vitamin D receptor and synergize with vitamin D, a known inhibitor of HC11 cell growth, was also investigated. HC11 cells expressed higher mRNA levels of both RAR a and RAR g when compared to HC11ras cells. In contrast, RAR ß, as well as RXR a, ß and g expression was low in both HC11 and HC11ras cells. In addition, RAR ß mRNA was induced by retinoic acid treatment in both cells. In spite of these observations, no effects were seen on cell proliferation or differentiation upon exposure to retinoic acid. Neither vitamin D receptor induction nor synergy with vitamin D on growth inhibition was observed. We conclude that the RAR expression profile could be related to the transformed state in HC11ras cells and that the retinoic acid resistance observed merits further investigation.
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spelling Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acidRetinoic acid receptorsMouse mammary cellsHC11ras cellsCarcinogenesisThe objective of the present study was to determine the effects of retinoic acid on the growth of the mouse mammary cells HC11 and HC11ras, which are a model for in vitro breast cancer progression. The expression of the two classes (RARs and RXRs) of retinoic acid receptor mRNAs was determined by Northern blot analysis. Receptor functional integrity was determined by testing whether RAR ß mRNA could be induced by retinoic acid. The effects of a 72-h exposure to 50 µM 13-cis retinoic acid on HC11 and HC11ras cell proliferation and HC11 cell differentiation were investigated by flow cytometric cell cycle analysis, and by determination of ß-casein mRNA expression, respectively. The possibility that retinoic acid would induce the expression of the vitamin D receptor and synergize with vitamin D, a known inhibitor of HC11 cell growth, was also investigated. HC11 cells expressed higher mRNA levels of both RAR a and RAR g when compared to HC11ras cells. In contrast, RAR ß, as well as RXR a, ß and g expression was low in both HC11 and HC11ras cells. In addition, RAR ß mRNA was induced by retinoic acid treatment in both cells. In spite of these observations, no effects were seen on cell proliferation or differentiation upon exposure to retinoic acid. Neither vitamin D receptor induction nor synergy with vitamin D on growth inhibition was observed. We conclude that the RAR expression profile could be related to the transformed state in HC11ras cells and that the retinoic acid resistance observed merits further investigation.Associação Brasileira de Divulgação Científica2003-12-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001200019Brazilian Journal of Medical and Biological Research v.36 n.12 2003reponame:Brazilian Journal of Medical and Biological Researchinstname:Associação Brasileira de Divulgação Científica (ABDC)instacron:ABDC10.1590/S0100-879X2003001200019info:eu-repo/semantics/openAccessSnitcovsky,I.Katayama,M.L.H.Folgueira,M.A.A.K.Brentani,M.M.eng2003-11-17T00:00:00Zoai:scielo:S0100-879X2003001200019Revistahttps://www.bjournal.org/https://old.scielo.br/oai/scielo-oai.phpbjournal@terra.com.br||bjournal@terra.com.br1414-431X0100-879Xopendoar:2003-11-17T00:00Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica (ABDC)false
dc.title.none.fl_str_mv Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid
title Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid
spellingShingle Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid
Snitcovsky,I.
Retinoic acid receptors
Mouse mammary cells
HC11ras cells
Carcinogenesis
title_short Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid
title_full Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid
title_fullStr Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid
title_full_unstemmed Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid
title_sort Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid
author Snitcovsky,I.
author_facet Snitcovsky,I.
Katayama,M.L.H.
Folgueira,M.A.A.K.
Brentani,M.M.
author_role author
author2 Katayama,M.L.H.
Folgueira,M.A.A.K.
Brentani,M.M.
author2_role author
author
author
dc.contributor.author.fl_str_mv Snitcovsky,I.
Katayama,M.L.H.
Folgueira,M.A.A.K.
Brentani,M.M.
dc.subject.por.fl_str_mv Retinoic acid receptors
Mouse mammary cells
HC11ras cells
Carcinogenesis
topic Retinoic acid receptors
Mouse mammary cells
HC11ras cells
Carcinogenesis
description The objective of the present study was to determine the effects of retinoic acid on the growth of the mouse mammary cells HC11 and HC11ras, which are a model for in vitro breast cancer progression. The expression of the two classes (RARs and RXRs) of retinoic acid receptor mRNAs was determined by Northern blot analysis. Receptor functional integrity was determined by testing whether RAR ß mRNA could be induced by retinoic acid. The effects of a 72-h exposure to 50 µM 13-cis retinoic acid on HC11 and HC11ras cell proliferation and HC11 cell differentiation were investigated by flow cytometric cell cycle analysis, and by determination of ß-casein mRNA expression, respectively. The possibility that retinoic acid would induce the expression of the vitamin D receptor and synergize with vitamin D, a known inhibitor of HC11 cell growth, was also investigated. HC11 cells expressed higher mRNA levels of both RAR a and RAR g when compared to HC11ras cells. In contrast, RAR ß, as well as RXR a, ß and g expression was low in both HC11 and HC11ras cells. In addition, RAR ß mRNA was induced by retinoic acid treatment in both cells. In spite of these observations, no effects were seen on cell proliferation or differentiation upon exposure to retinoic acid. Neither vitamin D receptor induction nor synergy with vitamin D on growth inhibition was observed. We conclude that the RAR expression profile could be related to the transformed state in HC11ras cells and that the retinoic acid resistance observed merits further investigation.
publishDate 2003
dc.date.none.fl_str_mv 2003-12-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001200019
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001200019
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/S0100-879X2003001200019
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Associação Brasileira de Divulgação Científica
publisher.none.fl_str_mv Associação Brasileira de Divulgação Científica
dc.source.none.fl_str_mv Brazilian Journal of Medical and Biological Research v.36 n.12 2003
reponame:Brazilian Journal of Medical and Biological Research
instname:Associação Brasileira de Divulgação Científica (ABDC)
instacron:ABDC
instname_str Associação Brasileira de Divulgação Científica (ABDC)
instacron_str ABDC
institution ABDC
reponame_str Brazilian Journal of Medical and Biological Research
collection Brazilian Journal of Medical and Biological Research
repository.name.fl_str_mv Brazilian Journal of Medical and Biological Research - Associação Brasileira de Divulgação Científica (ABDC)
repository.mail.fl_str_mv bjournal@terra.com.br||bjournal@terra.com.br
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