Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis

Target organ of metastasis determines the fate of metastasis. The soluble factors released from one or more cell types in the new stroma may influence growth and survival of metastatic cells. In the present study, we used conditioned media from the kidney, liver and lung, the latter being the target...

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Autores: Ladeda, Virginia, Adam, Alejandro P., Puricelli, Lydia Ines, Bal De Kier Joffé, Elisa
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2001
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/190770
Acceso en línea:http://hdl.handle.net/11336/190770
Access Level:acceso abierto
Palabra clave:APOPTOSIS
BREAST CANCER
MICROENVIRONMENT
ORGAN-SPECIFIC METASTASIS
SURVIVAL FACTORS
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
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repository_id_str
spelling Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasisLadeda, VirginiaAdam, Alejandro P.Puricelli, Lydia InesBal De Kier Joffé, ElisaAPOPTOSISBREAST CANCERMICROENVIRONMENTORGAN-SPECIFIC METASTASISSURVIVAL FACTORShttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Target organ of metastasis determines the fate of metastasis. The soluble factors released from one or more cell types in the new stroma may influence growth and survival of metastatic cells. In the present study, we used conditioned media from the kidney, liver and lung, the latter being the target organ of metastasis of murine mammary adenocarcinoma cell lines LM3, LMM3 and F3II, to assess whether the soluble factors released from these organs could modulate in vitro survival of these cell lines after apoptosis-inducing treatments and to investigate the mechanisms involved in this effect. We demonstrate that conditioned medium from lung, but not from liver or kidney, promotes survival of these cells after doxorubicin, cisplatin, agonistic anti-Fas antibody and serum withdrawal treatments. Furthermore, LMM3 cells treated with lung conditioned medium after doxorubicin exposure maintained their tumorigenic capacity and metastatic potential. Neither IGF nor EGF could promote survival but, surprisingly, TGF-β could reduce sensitivity of LMM3 cells to doxorubicin in vitro. Doxorubicin treatment induced Bax expression and down-regulated Bcl-2 expression. In contrast, lung conditioned medium increased Bcl-2 expression and inhibited doxorubicin-mediated Bcl-2 down-regulation. Neither of those treatments alone modified Bcl-xL expression, although co-treatment induced a 3- to 5-fold increase of its expression. These results suggest that the lung microenvironment could promote metastasis of these adenocarcinoma cell lines by increasing survival of metastatic cells, possibly by modulation of Bcl-2 protein family expression.Fil: Ladeda, Virginia. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; ArgentinaFil: Adam, Alejandro P.. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; ArgentinaFil: Puricelli, Lydia Ines. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Bal De Kier Joffé, Elisa. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; ArgentinaSpringer2001-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/mswordapplication/pdfhttp://hdl.handle.net/11336/190770Ladeda, Virginia; Adam, Alejandro P.; Puricelli, Lydia Ines; Bal De Kier Joffé, Elisa; Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis; Springer; Breast Cancer Research and Treatment; 69; 1; 12-2001; 39-510167-6806CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1023/a:1012201805486info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1023/A:1012201805486info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2024-05-08T13:43:49Zoai:ri.conicet.gov.ar:11336/190770instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982024-05-08 13:43:49.829CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis
title Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis
spellingShingle Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis
Ladeda, Virginia
APOPTOSIS
BREAST CANCER
MICROENVIRONMENT
ORGAN-SPECIFIC METASTASIS
SURVIVAL FACTORS
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
title_short Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis
title_full Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis
title_fullStr Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis
title_full_unstemmed Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis
title_sort Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis
dc.creator.none.fl_str_mv Ladeda, Virginia
Adam, Alejandro P.
Puricelli, Lydia Ines
Bal De Kier Joffé, Elisa
author Ladeda, Virginia
author_facet Ladeda, Virginia
Adam, Alejandro P.
Puricelli, Lydia Ines
Bal De Kier Joffé, Elisa
author_role author
author2 Adam, Alejandro P.
Puricelli, Lydia Ines
Bal De Kier Joffé, Elisa
author2_role author
author
author
dc.subject.none.fl_str_mv APOPTOSIS
BREAST CANCER
MICROENVIRONMENT
ORGAN-SPECIFIC METASTASIS
SURVIVAL FACTORS
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
topic APOPTOSIS
BREAST CANCER
MICROENVIRONMENT
ORGAN-SPECIFIC METASTASIS
SURVIVAL FACTORS
https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
description Target organ of metastasis determines the fate of metastasis. The soluble factors released from one or more cell types in the new stroma may influence growth and survival of metastatic cells. In the present study, we used conditioned media from the kidney, liver and lung, the latter being the target organ of metastasis of murine mammary adenocarcinoma cell lines LM3, LMM3 and F3II, to assess whether the soluble factors released from these organs could modulate in vitro survival of these cell lines after apoptosis-inducing treatments and to investigate the mechanisms involved in this effect. We demonstrate that conditioned medium from lung, but not from liver or kidney, promotes survival of these cells after doxorubicin, cisplatin, agonistic anti-Fas antibody and serum withdrawal treatments. Furthermore, LMM3 cells treated with lung conditioned medium after doxorubicin exposure maintained their tumorigenic capacity and metastatic potential. Neither IGF nor EGF could promote survival but, surprisingly, TGF-β could reduce sensitivity of LMM3 cells to doxorubicin in vitro. Doxorubicin treatment induced Bax expression and down-regulated Bcl-2 expression. In contrast, lung conditioned medium increased Bcl-2 expression and inhibited doxorubicin-mediated Bcl-2 down-regulation. Neither of those treatments alone modified Bcl-xL expression, although co-treatment induced a 3- to 5-fold increase of its expression. These results suggest that the lung microenvironment could promote metastasis of these adenocarcinoma cell lines by increasing survival of metastatic cells, possibly by modulation of Bcl-2 protein family expression.
publishDate 2001
dc.date.none.fl_str_mv 2001-12
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/190770
Ladeda, Virginia; Adam, Alejandro P.; Puricelli, Lydia Ines; Bal De Kier Joffé, Elisa; Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis; Springer; Breast Cancer Research and Treatment; 69; 1; 12-2001; 39-51
0167-6806
CONICET Digital
CONICET
url http://hdl.handle.net/11336/190770
identifier_str_mv Ladeda, Virginia; Adam, Alejandro P.; Puricelli, Lydia Ines; Bal De Kier Joffé, Elisa; Apoptotic cell death in mammary adenocarcinoma cells is prevented by soluble factors present in the target organ of metastasis; Springer; Breast Cancer Research and Treatment; 69; 1; 12-2001; 39-51
0167-6806
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1023/a:1012201805486
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1023/A:1012201805486
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/msword
application/pdf
dc.publisher.none.fl_str_mv Springer
publisher.none.fl_str_mv Springer
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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