TNF-α/IL-1/NF-κB transduction pathway in human cancer prostate

TNFα exerts apoptosis throughout an intracellular transduction pathway that involves the kinase proteins TRAF-2 (integration point of apoptotic and survival signals), ASK1 (pro-apoptotic protein), MEK-4 (p38 activator and metastasis suppressor gene), JNK (stress mitogen activated protein kinase) and...

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Detalles Bibliográficos
Autores: Paniagua Gómez-Álvarez, Ricardo, Royuela García, María del Mar|||0000-0003-1999-9849, Fraile Laiz, Benito|||0000-0002-4847-055X, Rodríguez Berriguete, Gonzalo
Tipo de recurso: artículo
Fecha de publicación:2008
País:España
Institución:Universidad de Alcalá (UAH)
Repositorio:e_Buah Biblioteca Digital Universidad de Alcalá
Idioma:inglés
OAI Identifier:oai:ebuah.uah.es:10017/32678
Acceso en línea:http://hdl.handle.net/10017/32678
https://dx.doi.org/10.14670/HH-23.1279
Access Level:acceso abierto
Palabra clave:Prostate carcinoma
IL-1
TNF-α
NF-κB
NIK
p38
Antineoplastic Agents/therapeutic use
Apoptosis
Cell Proliferation
Cell Survival
Humans
Interleukin-1/antagonists & inhibitors
Interleukin-1/metabolism
Male
NF-kappa B/metabolism
Prostatic Neoplasms/drug therapy
Prostatic Neoplasms/metabolism
Prostatic Neoplasms/pathology
Protein-Serine-Threonine Kinases/metabolism
Signal Transduction/drug effects
Transcription Factor AP-1/metabolism
Tumor Necrosis Factor-alpha/antagonists & inhibitors
Tumor Necrosis Factor-alpha/metabolism
p38 Mitogen-Activated Protein Kinases/metabolism
Biología
Genética
Ciencia
Biology
Genetics
Science
Descripción
Sumario:TNFα exerts apoptosis throughout an intracellular transduction pathway that involves the kinase proteins TRAF-2 (integration point of apoptotic and survival signals), ASK1 (pro-apoptotic protein), MEK-4 (p38 activator and metastasis suppressor gene), JNK (stress mitogen activated protein kinase) and the transcription factor AP-1. TNFα also exerts proliferation by p38 activation, or when TRAF-2 simultaneously induces the transcription factor NF-κB by NIK. NIK and p38 may also be activated by IL-1. P38 activated several transcription factors such as Elk-1, ATF-2 and NF-κB. NIK also may activate NF-κB. The aim of the present article was to evaluate the different components of this TNFα/IL-1 transduction pathway in human prostate carcinoma (PC) in comparison with normal human prostate. In prostate cancer, pro-apoptotic TNFα/AP-1 pathway is probably inactivated by different factors such as p21 (at ASK-1 level) and bcl-2 (at JNK level), or diverted towards p38 or NIK activation. IL-1α enhances proliferation through IL-1RI that activates either NIK or p38 transduction pathway. P38 and NIK activate different transcription factors related with cell proliferation and survival such as ATF-2, Elk-1 or NF-κB. In order to search a possible target to cancer prostate treatment we proposed that inhibition of several proinflamatory cytokines such as IL-1 and TNFα might be a possible target for PC treatment, because decrease the activity of all transduction pathway members that activate transcription factors as NF-κB, Elk-1 or ATF-2.