Normal HC11 and ras-transformed mouse mammary cells are resistant to the antiproliferative effects of retinoic acid
Autor(a) principal: | |
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Data de Publicação: | 2003 |
Outros Autores: | , , |
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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Brazilian Journal of Medical and Biological Research |
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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 |
_version_ |
1754302932603371520 |