PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer

Autores
Mauro, Laura Valeria; Grossoni, Valeria C.; Urtreger, Alejandro Jorge; Yang, Chengfen; Colombo, Lucas Luis; Morandi, Ana; Pallota, María G.; Kazanietz, Marcelo G.; Bal, Elisa Dora; Puricelli, Lydia Ines
Año de publicación
2010
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
OBJECTIVE: Our objective was to study the role of protein kinase C delta (PKCdelta) in the progression of human pancreatic carcinoma. METHODS: Protein kinase C delta expression in human ductal carcinoma (n = 22) was studied by immunohistochemistry. We analyzed the effect of PKCdelta overexpression on in vivo and in vitro properties of human ductal carcinoma cell line PANC1. RESULTS: Human ductal carcinomas showed PKCdelta overexpression compared with normal counterparts. In addition, in vitro PKCdelta-PANC1 cells showed increased anchorage-independent growth and higher resistance to serum starvation and to treatment with cytotoxic drugs. Using pharmacological inhibitors, we determined that phosphatidylinositol-3-kinase and extracellular receptor kinase pathways were involved in the proliferation of PKCdelta-PANC1. Interestingly, PKCdelta-PANC1 cells showed a less in vitro invasive ability and an impairment in their ability to migrate and to secrete the proteolytic enzyme matrix metalloproteinase-2. In vivo experiments indicated that PKCdelta-PANC1 cells were more tumorigenic, as they developed tumors with a significantly lower latency and a higher growth rate with respect to the tumors generated with control cells. Besides, only PKCdelta-PANC1 cells developed lung metastasis. CONCLUSION: Our results showed that the overexpression of PKCdelta in PANC1 cells induced a more malignant phenotype in vivo, probably through the modulation of cell proliferation and survival, involving phosphatidylinositol-3-kinase and extracellular receptor kinase signaling pathways.
Fil: Mauro, Laura Valeria. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Grossoni, Valeria C.. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina
Fil: Urtreger, Alejandro Jorge. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Yang, Chengfen. Michigan State University; Estados Unidos
Fil: Colombo, Lucas Luis. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Morandi, Ana. Hospital Italiano de Buenos Aires; Argentina
Fil: Pallota, María G.. Hospital Italiano de Buenos Aires; Argentina
Fil: Kazanietz, Marcelo G.. State University Of Pennsylvania; Estados Unidos
Fil: Bal, Elisa Dora. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Puricelli, Lydia Ines. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Materia
Human Pancreatic Adenocarcinoma
Pkcδ
Invasion
Pi3k/Akt
Erk
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/14494
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/14494
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancerMauro, Laura ValeriaGrossoni, Valeria C.Urtreger, Alejandro JorgeYang, ChengfenColombo, Lucas LuisMorandi, AnaPallota, María G.Kazanietz, Marcelo G.Bal, Elisa DoraPuricelli, Lydia InesHuman Pancreatic AdenocarcinomaPkcδInvasionPi3k/AktErkhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1OBJECTIVE: Our objective was to study the role of protein kinase C delta (PKCdelta) in the progression of human pancreatic carcinoma. METHODS: Protein kinase C delta expression in human ductal carcinoma (n = 22) was studied by immunohistochemistry. We analyzed the effect of PKCdelta overexpression on in vivo and in vitro properties of human ductal carcinoma cell line PANC1. RESULTS: Human ductal carcinomas showed PKCdelta overexpression compared with normal counterparts. In addition, in vitro PKCdelta-PANC1 cells showed increased anchorage-independent growth and higher resistance to serum starvation and to treatment with cytotoxic drugs. Using pharmacological inhibitors, we determined that phosphatidylinositol-3-kinase and extracellular receptor kinase pathways were involved in the proliferation of PKCdelta-PANC1. Interestingly, PKCdelta-PANC1 cells showed a less in vitro invasive ability and an impairment in their ability to migrate and to secrete the proteolytic enzyme matrix metalloproteinase-2. In vivo experiments indicated that PKCdelta-PANC1 cells were more tumorigenic, as they developed tumors with a significantly lower latency and a higher growth rate with respect to the tumors generated with control cells. Besides, only PKCdelta-PANC1 cells developed lung metastasis. CONCLUSION: Our results showed that the overexpression of PKCdelta in PANC1 cells induced a more malignant phenotype in vivo, probably through the modulation of cell proliferation and survival, involving phosphatidylinositol-3-kinase and extracellular receptor kinase signaling pathways.Fil: Mauro, Laura Valeria. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Grossoni, Valeria C.. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; ArgentinaFil: Urtreger, Alejandro Jorge. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Yang, Chengfen. Michigan State University; Estados UnidosFil: Colombo, Lucas Luis. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Morandi, Ana. Hospital Italiano de Buenos Aires; ArgentinaFil: Pallota, María G.. Hospital Italiano de Buenos Aires; ArgentinaFil: Kazanietz, Marcelo G.. State University Of Pennsylvania; Estados UnidosFil: Bal, Elisa Dora. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Puricelli, Lydia Ines. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaLippincott Williams2010-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/14494Mauro, Laura Valeria; Grossoni, Valeria C.; Urtreger, Alejandro Jorge; Yang, Chengfen; Colombo, Lucas Luis; et al.; PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer; Lippincott Williams; Pancreas; 39; 1; 1-2010; e31-410885-3177enginfo:eu-repo/semantics/altIdentifier/url/http://journals.lww.com/pancreasjournal/pages/articleviewer.aspx?year=2010&issue=01000&article=00035&type=abstractinfo:eu-repo/semantics/altIdentifier/doi/10.1097/MPA.0b013e3181bce796info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:35:49Zoai:ri.conicet.gov.ar:11336/14494instacron: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:34982025-09-29 10:35:50.077CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer
title PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer
spellingShingle PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer
Mauro, Laura Valeria
Human Pancreatic Adenocarcinoma
Pkcδ
Invasion
Pi3k/Akt
Erk
title_short PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer
title_full PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer
title_fullStr PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer
title_full_unstemmed PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer
title_sort PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer
dc.creator.none.fl_str_mv Mauro, Laura Valeria
Grossoni, Valeria C.
Urtreger, Alejandro Jorge
Yang, Chengfen
Colombo, Lucas Luis
Morandi, Ana
Pallota, María G.
Kazanietz, Marcelo G.
Bal, Elisa Dora
Puricelli, Lydia Ines
author Mauro, Laura Valeria
author_facet Mauro, Laura Valeria
Grossoni, Valeria C.
Urtreger, Alejandro Jorge
Yang, Chengfen
Colombo, Lucas Luis
Morandi, Ana
Pallota, María G.
Kazanietz, Marcelo G.
Bal, Elisa Dora
Puricelli, Lydia Ines
author_role author
author2 Grossoni, Valeria C.
Urtreger, Alejandro Jorge
Yang, Chengfen
Colombo, Lucas Luis
Morandi, Ana
Pallota, María G.
Kazanietz, Marcelo G.
Bal, Elisa Dora
Puricelli, Lydia Ines
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Human Pancreatic Adenocarcinoma
Pkcδ
Invasion
Pi3k/Akt
Erk
topic Human Pancreatic Adenocarcinoma
Pkcδ
Invasion
Pi3k/Akt
Erk
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv OBJECTIVE: Our objective was to study the role of protein kinase C delta (PKCdelta) in the progression of human pancreatic carcinoma. METHODS: Protein kinase C delta expression in human ductal carcinoma (n = 22) was studied by immunohistochemistry. We analyzed the effect of PKCdelta overexpression on in vivo and in vitro properties of human ductal carcinoma cell line PANC1. RESULTS: Human ductal carcinomas showed PKCdelta overexpression compared with normal counterparts. In addition, in vitro PKCdelta-PANC1 cells showed increased anchorage-independent growth and higher resistance to serum starvation and to treatment with cytotoxic drugs. Using pharmacological inhibitors, we determined that phosphatidylinositol-3-kinase and extracellular receptor kinase pathways were involved in the proliferation of PKCdelta-PANC1. Interestingly, PKCdelta-PANC1 cells showed a less in vitro invasive ability and an impairment in their ability to migrate and to secrete the proteolytic enzyme matrix metalloproteinase-2. In vivo experiments indicated that PKCdelta-PANC1 cells were more tumorigenic, as they developed tumors with a significantly lower latency and a higher growth rate with respect to the tumors generated with control cells. Besides, only PKCdelta-PANC1 cells developed lung metastasis. CONCLUSION: Our results showed that the overexpression of PKCdelta in PANC1 cells induced a more malignant phenotype in vivo, probably through the modulation of cell proliferation and survival, involving phosphatidylinositol-3-kinase and extracellular receptor kinase signaling pathways.
Fil: Mauro, Laura Valeria. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Grossoni, Valeria C.. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina
Fil: Urtreger, Alejandro Jorge. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Yang, Chengfen. Michigan State University; Estados Unidos
Fil: Colombo, Lucas Luis. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Morandi, Ana. Hospital Italiano de Buenos Aires; Argentina
Fil: Pallota, María G.. Hospital Italiano de Buenos Aires; Argentina
Fil: Kazanietz, Marcelo G.. State University Of Pennsylvania; Estados Unidos
Fil: Bal, Elisa Dora. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Puricelli, Lydia Ines. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncologia "Angel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
description OBJECTIVE: Our objective was to study the role of protein kinase C delta (PKCdelta) in the progression of human pancreatic carcinoma. METHODS: Protein kinase C delta expression in human ductal carcinoma (n = 22) was studied by immunohistochemistry. We analyzed the effect of PKCdelta overexpression on in vivo and in vitro properties of human ductal carcinoma cell line PANC1. RESULTS: Human ductal carcinomas showed PKCdelta overexpression compared with normal counterparts. In addition, in vitro PKCdelta-PANC1 cells showed increased anchorage-independent growth and higher resistance to serum starvation and to treatment with cytotoxic drugs. Using pharmacological inhibitors, we determined that phosphatidylinositol-3-kinase and extracellular receptor kinase pathways were involved in the proliferation of PKCdelta-PANC1. Interestingly, PKCdelta-PANC1 cells showed a less in vitro invasive ability and an impairment in their ability to migrate and to secrete the proteolytic enzyme matrix metalloproteinase-2. In vivo experiments indicated that PKCdelta-PANC1 cells were more tumorigenic, as they developed tumors with a significantly lower latency and a higher growth rate with respect to the tumors generated with control cells. Besides, only PKCdelta-PANC1 cells developed lung metastasis. CONCLUSION: Our results showed that the overexpression of PKCdelta in PANC1 cells induced a more malignant phenotype in vivo, probably through the modulation of cell proliferation and survival, involving phosphatidylinositol-3-kinase and extracellular receptor kinase signaling pathways.
publishDate 2010
dc.date.none.fl_str_mv 2010-01
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/11336/14494
Mauro, Laura Valeria; Grossoni, Valeria C.; Urtreger, Alejandro Jorge; Yang, Chengfen; Colombo, Lucas Luis; et al.; PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer; Lippincott Williams; Pancreas; 39; 1; 1-2010; e31-41
0885-3177
url http://hdl.handle.net/11336/14494
identifier_str_mv Mauro, Laura Valeria; Grossoni, Valeria C.; Urtreger, Alejandro Jorge; Yang, Chengfen; Colombo, Lucas Luis; et al.; PKC delta (PKCδ) promotes tumoral progression of human ductal pancreatic cancer; Lippincott Williams; Pancreas; 39; 1; 1-2010; e31-41
0885-3177
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://journals.lww.com/pancreasjournal/pages/articleviewer.aspx?year=2010&issue=01000&article=00035&type=abstract
info:eu-repo/semantics/altIdentifier/doi/10.1097/MPA.0b013e3181bce796
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/pdf
dc.publisher.none.fl_str_mv Lippincott Williams
publisher.none.fl_str_mv Lippincott Williams
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
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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score 13.070432

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