Silencing of the integrin-linked kinase gene suppresses the proliferation, migration and invasion of pancreatic cancer cells (Panc-1)

Detalhes bibliográficos
Autor(a) principal: Zhu,Xiang-Yu
Data de Publicação: 2012
Outros Autores: Liu,Ning, Liu,Wei, Song,Shao-Wei, Guo,Ke-Jian
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Genetics and Molecular Biology
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572012000300022
Resumo: Integrin-linked kinase (ILK) is an ankyrin repeat-containing serine-threonine protein kinase that is involved in the regulation of integrin-mediated processes such as cancer cell proliferation, migration and invasion. In this study, we examined the effect of a lentivirus-mediated knockdown of ILK on the proliferation, migration and invasion of pancreatic cancer (Panc-1) cells. Immunohistochemical staining showed that ILK expression was enhanced in pancreatic cancer tissue. The silencing of ILK in human Panc-1 cells led to cell cycle arrest in the G0/G1 phase and delayed cell proliferation, in addition to down-regulating cell migration and invasion. The latter effects were mediated by up-regulating the expression of E-cadherin, a key protein in cell adhesion. These findings indicate that ILK may be a new diagnostic marker for pancreatic cancer and that silencing ILK could be a potentially useful therapeutic approach for treating pancreatic cancer.
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spelling Silencing of the integrin-linked kinase gene suppresses the proliferation, migration and invasion of pancreatic cancer cells (Panc-1)E-cadherinepithelial-mesenchymal transition (EMT)integrin-linked kinase (ILK)Panc-1 cell lineRNA interference (RNAi)Integrin-linked kinase (ILK) is an ankyrin repeat-containing serine-threonine protein kinase that is involved in the regulation of integrin-mediated processes such as cancer cell proliferation, migration and invasion. In this study, we examined the effect of a lentivirus-mediated knockdown of ILK on the proliferation, migration and invasion of pancreatic cancer (Panc-1) cells. Immunohistochemical staining showed that ILK expression was enhanced in pancreatic cancer tissue. The silencing of ILK in human Panc-1 cells led to cell cycle arrest in the G0/G1 phase and delayed cell proliferation, in addition to down-regulating cell migration and invasion. The latter effects were mediated by up-regulating the expression of E-cadherin, a key protein in cell adhesion. These findings indicate that ILK may be a new diagnostic marker for pancreatic cancer and that silencing ILK could be a potentially useful therapeutic approach for treating pancreatic cancer.Sociedade Brasileira de Genética2012-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572012000300022Genetics and Molecular Biology v.35 n.2 2012reponame:Genetics and Molecular Biologyinstname:Sociedade Brasileira de Genética (SBG)instacron:SBG10.1590/S1415-47572012005000028info:eu-repo/semantics/openAccessZhu,Xiang-YuLiu,NingLiu,WeiSong,Shao-WeiGuo,Ke-Jianeng2012-06-19T00:00:00Zoai:scielo:S1415-47572012000300022Revistahttp://www.gmb.org.br/ONGhttps://old.scielo.br/oai/scielo-oai.php||editor@gmb.org.br1678-46851415-4757opendoar:2012-06-19T00:00Genetics and Molecular Biology - Sociedade Brasileira de Genética (SBG)false
dc.title.none.fl_str_mv Silencing of the integrin-linked kinase gene suppresses the proliferation, migration and invasion of pancreatic cancer cells (Panc-1)
title Silencing of the integrin-linked kinase gene suppresses the proliferation, migration and invasion of pancreatic cancer cells (Panc-1)
spellingShingle Silencing of the integrin-linked kinase gene suppresses the proliferation, migration and invasion of pancreatic cancer cells (Panc-1)
Zhu,Xiang-Yu
E-cadherin
epithelial-mesenchymal transition (EMT)
integrin-linked kinase (ILK)
Panc-1 cell line
RNA interference (RNAi)
title_short Silencing of the integrin-linked kinase gene suppresses the proliferation, migration and invasion of pancreatic cancer cells (Panc-1)
title_full Silencing of the integrin-linked kinase gene suppresses the proliferation, migration and invasion of pancreatic cancer cells (Panc-1)
title_fullStr Silencing of the integrin-linked kinase gene suppresses the proliferation, migration and invasion of pancreatic cancer cells (Panc-1)
title_full_unstemmed Silencing of the integrin-linked kinase gene suppresses the proliferation, migration and invasion of pancreatic cancer cells (Panc-1)
title_sort Silencing of the integrin-linked kinase gene suppresses the proliferation, migration and invasion of pancreatic cancer cells (Panc-1)
author Zhu,Xiang-Yu
author_facet Zhu,Xiang-Yu
Liu,Ning
Liu,Wei
Song,Shao-Wei
Guo,Ke-Jian
author_role author
author2 Liu,Ning
Liu,Wei
Song,Shao-Wei
Guo,Ke-Jian
author2_role author
author
author
author
dc.contributor.author.fl_str_mv Zhu,Xiang-Yu
Liu,Ning
Liu,Wei
Song,Shao-Wei
Guo,Ke-Jian
dc.subject.por.fl_str_mv E-cadherin
epithelial-mesenchymal transition (EMT)
integrin-linked kinase (ILK)
Panc-1 cell line
RNA interference (RNAi)
topic E-cadherin
epithelial-mesenchymal transition (EMT)
integrin-linked kinase (ILK)
Panc-1 cell line
RNA interference (RNAi)
description Integrin-linked kinase (ILK) is an ankyrin repeat-containing serine-threonine protein kinase that is involved in the regulation of integrin-mediated processes such as cancer cell proliferation, migration and invasion. In this study, we examined the effect of a lentivirus-mediated knockdown of ILK on the proliferation, migration and invasion of pancreatic cancer (Panc-1) cells. Immunohistochemical staining showed that ILK expression was enhanced in pancreatic cancer tissue. The silencing of ILK in human Panc-1 cells led to cell cycle arrest in the G0/G1 phase and delayed cell proliferation, in addition to down-regulating cell migration and invasion. The latter effects were mediated by up-regulating the expression of E-cadherin, a key protein in cell adhesion. These findings indicate that ILK may be a new diagnostic marker for pancreatic cancer and that silencing ILK could be a potentially useful therapeutic approach for treating pancreatic cancer.
publishDate 2012
dc.date.none.fl_str_mv 2012-01-01
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=S1415-47572012000300022
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572012000300022
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/S1415-47572012005000028
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 Sociedade Brasileira de Genética
publisher.none.fl_str_mv Sociedade Brasileira de Genética
dc.source.none.fl_str_mv Genetics and Molecular Biology v.35 n.2 2012
reponame:Genetics and Molecular Biology
instname:Sociedade Brasileira de Genética (SBG)
instacron:SBG
instname_str Sociedade Brasileira de Genética (SBG)
instacron_str SBG
institution SBG
reponame_str Genetics and Molecular Biology
collection Genetics and Molecular Biology
repository.name.fl_str_mv Genetics and Molecular Biology - Sociedade Brasileira de Genética (SBG)
repository.mail.fl_str_mv ||editor@gmb.org.br
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