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dc.creatorAnton, I. (Iker)-
dc.creatorMolina, E. (Eva)-
dc.creatorLuis-Ravelo, D. (Diego)-
dc.creatorZandueta, C. (Carolina)-
dc.creatorValencia, K. (Karmele)-
dc.creatorOrmazábal, C. (Cristina)-
dc.creatorMartinez-Canarias, S. (Susana)-
dc.creatorPerurena, N. (Naiara)-
dc.creatorPajares, M.J. (María José)-
dc.creatorAgorreta, J. (Jackeline)-
dc.creatorMontuenga-Badia, L.M. (Luis M.)-
dc.creatorSegura, V. (Víctor)-
dc.creatorWistuba, I.I. (Ignacio I.)-
dc.creatorRivas, J. (Javier) de las-
dc.creatorHermida, J. (José)-
dc.creatorLecanda, F. (Fernando)-
dc.date.accessioned2012-05-09T11:08:52Z-
dc.date.available2012-05-09T11:08:52Z-
dc.date.issued2012-
dc.identifier.citationAnton I, Molina E, Luis-Ravelo D, Zandueta C, Valencia K, Ormazabal C, et al. Receptor of Activated Protein C Promotes Metastasis and Correlates with Clinical Outcome in Lung Adenocarcinoma. Am J Respir Crit Care Med 2012 Mar 29.es_ES
dc.identifier.issn1535-4970-
dc.identifier.urihttps://hdl.handle.net/10171/21974-
dc.description.abstractRATIONALE: Efficient metastasis requires survival and adaptation of tumor cells to stringent conditions imposed by the extracellular milieu. Identification of critical survival signaling pathways in tumor cells might unveil novel targets relevant in disease progression. OBJECTIVES: To investigate the contribution of activated protein C (APC) and its receptor (EPCR) in animal models of lung cancer metastasis and in patients with lung adenocarcinoma. METHODS: Signaling pathway triggered by APC/EPCR and its relevance in apoptosis was studied in vitro. Functional significance was assessed by silencing and blocking antibodies in several in vivo models of lung cancer metastasis. We examined EPCR levels using a microarray dataset of 107 patients. Immunohistochemical analysis was performed in an independent cohort of 295 patients with lung adenocarcinoma. MEASUREMENTS AND MAIN RESULTS: The effects of APC binding to EPCR rapidly triggered Akt and ERK signaling pathways, leading to attenuated in vitro apoptosis. In vivo, silencing of EPCR expression or blocking APC/EPCR interaction reduced homing resulting in impaired prometastatic activity. Moreover, overexpression of EPCR induced an increase metastatic activity to target organs. Analysis of clinical samples showed a robust association between high EPCR levels and poor prognosis particularly in stage I patients. CONCLUSIONS: EPCR and its ligand APC promote cell survival that contributes to tumor cell endurance to stress favoring prometastatic activity of lung adenocarcinoma (ADC). EPCR/APC is a novel target of relevance in the clinical outcome of early-stage lung cancer.es_ES
dc.language.isoenges_ES
dc.publisherAmerican Thoracic Societyes_ES
dc.rightsinfo:eu-repo/semantics/closedAccess-
dc.subjectSurvivales_ES
dc.subjectMicroenvironmentes_ES
dc.subjectBone Metastasises_ES
dc.subjectPrognosises_ES
dc.subjectAdrenal glandes_ES
dc.titleReceptor of Activated Protein C Promotes Metastasis and Correlates with Clinical Outcome in Lung Adenocarcinomaes_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherversionhttp://ajrccm.atsjournals.org/content/early/2012/03/28/rccm.201110-1826OCes_ES
dc.type.driverinfo:eu-repo/semantics/articlees_ES

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