Dysregulation of apoptosis in hepatocellular carcinoma cells

Hepatocellular carcinoma (HCC) is a major health problem, being the sixth most common cancer world-wide. Dysregulation of the balance between proliferation and cell death represents a pro-tumorigenic principle in human hepatocarcinogenesis. This review updates the recent relevant contributions repor...

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Detalhes bibliográficos
Autor: Fabregat Romero, Isabel
Formato: artículo
Estado:Versión publicada
Fecha de publicación:2009
País:España
Recursos:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/36457
Acesso em linha:https://hdl.handle.net/2445/36457
Access Level:acceso abierto
Palavra-chave:Apoptosi
Càncer de fetge
Apoptosis
Liver cancer
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spelling Dysregulation of apoptosis in hepatocellular carcinoma cellsFabregat Romero, IsabelApoptosiCàncer de fetgeApoptosisLiver cancerHepatocellular carcinoma (HCC) is a major health problem, being the sixth most common cancer world-wide. Dysregulation of the balance between proliferation and cell death represents a pro-tumorigenic principle in human hepatocarcinogenesis. This review updates the recent relevant contributions reporting molecular alterations for HCC that induce an imbalance in the regulation of apoptosis. Alterations in the expression and/or activation of p53 are frequent in HCC cells, which confer on them resistance to chemotherapeutic drugs. Many HCCs are also insensitive to apoptosis induced either by death receptor ligands, such as FasL or TRAIL, or by transforming growth factor-beta (TGF-beta). Although the expression of some pro-apoptotic genes is decreased, the balance between death and survival is dysregulated in HCC mainly due to overactivation of anti-apoptotic pathways. Indeed, some molecules involved in counteracting apoptosis, such as Bcl-XL, Mcl-1, c-IAP1, XIAP or survivin are over-expressed in HCC cells. Furthermore, some growth factors that mediate cell survival are up-regulated in HCC, as well as the molecules involved in the machinery responsible for cleavage of their pro-forms to an active peptide. The expression and/or activation of the JAK/STAT, PI3K/AKT and RAS/ERKs pathways are enhanced in many HCC cells, conferring on them resistance to apoptotic stimuli. Finally, recent evidence indicates that inflammatory processes, as well as the epithelial-mesenchymal transitions that occur in HCC cells to facilitate their dissemination, are related to cell survival. Therefore, therapeutic strategies to selectively inhibit anti-apoptotic signals in liver tumor cells have the potential to provide powerful tools to treat HCC.Baishideng Publishing Group2009info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://hdl.handle.net/2445/36457Articles publicats en revistes (Ciències Fisiològiques)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésReproducció del document publicat a: http://dx.doi.org/10.3748/wjg.15.513World Journal of Gastroenterology, 2009, vol. 15, num. 5, p. 513-520http://dx.doi.org/10.3748/wjg.15.513cc-by-nc (c) Fabregat Romero, Isabel, 2009http://creativecommons.org/licenses/by-nc/3.0/esinfo:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/364572026-05-27T06:46:51Z
dc.title.none.fl_str_mv Dysregulation of apoptosis in hepatocellular carcinoma cells
title Dysregulation of apoptosis in hepatocellular carcinoma cells
spellingShingle Dysregulation of apoptosis in hepatocellular carcinoma cells
Fabregat Romero, Isabel
Apoptosi
Càncer de fetge
Apoptosis
Liver cancer
title_short Dysregulation of apoptosis in hepatocellular carcinoma cells
title_full Dysregulation of apoptosis in hepatocellular carcinoma cells
title_fullStr Dysregulation of apoptosis in hepatocellular carcinoma cells
title_full_unstemmed Dysregulation of apoptosis in hepatocellular carcinoma cells
title_sort Dysregulation of apoptosis in hepatocellular carcinoma cells
dc.creator.none.fl_str_mv Fabregat Romero, Isabel
author Fabregat Romero, Isabel
author_facet Fabregat Romero, Isabel
author_role author
dc.subject.none.fl_str_mv Apoptosi
Càncer de fetge
Apoptosis
Liver cancer
topic Apoptosi
Càncer de fetge
Apoptosis
Liver cancer
description Hepatocellular carcinoma (HCC) is a major health problem, being the sixth most common cancer world-wide. Dysregulation of the balance between proliferation and cell death represents a pro-tumorigenic principle in human hepatocarcinogenesis. This review updates the recent relevant contributions reporting molecular alterations for HCC that induce an imbalance in the regulation of apoptosis. Alterations in the expression and/or activation of p53 are frequent in HCC cells, which confer on them resistance to chemotherapeutic drugs. Many HCCs are also insensitive to apoptosis induced either by death receptor ligands, such as FasL or TRAIL, or by transforming growth factor-beta (TGF-beta). Although the expression of some pro-apoptotic genes is decreased, the balance between death and survival is dysregulated in HCC mainly due to overactivation of anti-apoptotic pathways. Indeed, some molecules involved in counteracting apoptosis, such as Bcl-XL, Mcl-1, c-IAP1, XIAP or survivin are over-expressed in HCC cells. Furthermore, some growth factors that mediate cell survival are up-regulated in HCC, as well as the molecules involved in the machinery responsible for cleavage of their pro-forms to an active peptide. The expression and/or activation of the JAK/STAT, PI3K/AKT and RAS/ERKs pathways are enhanced in many HCC cells, conferring on them resistance to apoptotic stimuli. Finally, recent evidence indicates that inflammatory processes, as well as the epithelial-mesenchymal transitions that occur in HCC cells to facilitate their dissemination, are related to cell survival. Therefore, therapeutic strategies to selectively inhibit anti-apoptotic signals in liver tumor cells have the potential to provide powerful tools to treat HCC.
publishDate 2009
dc.date.none.fl_str_mv 2009
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/36457
url https://hdl.handle.net/2445/36457
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reproducció del document publicat a: http://dx.doi.org/10.3748/wjg.15.513
World Journal of Gastroenterology, 2009, vol. 15, num. 5, p. 513-520
http://dx.doi.org/10.3748/wjg.15.513
dc.rights.none.fl_str_mv cc-by-nc (c) Fabregat Romero, Isabel, 2009
http://creativecommons.org/licenses/by-nc/3.0/es
info:eu-repo/semantics/openAccess
rights_invalid_str_mv cc-by-nc (c) Fabregat Romero, Isabel, 2009
http://creativecommons.org/licenses/by-nc/3.0/es
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Baishideng Publishing Group
publisher.none.fl_str_mv Baishideng Publishing Group
dc.source.none.fl_str_mv Articles publicats en revistes (Ciències Fisiològiques)
reponame:Dipòsit Digital de la UB
instname:Universidad de Barcelona
instname_str Universidad de Barcelona
reponame_str Dipòsit Digital de la UB
collection Dipòsit Digital de la UB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,300719

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