PGA1-induced apoptosis involves specific activation of H-Ras and N-Ras in cellular endomembranes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-07-28

AUTHORS

B Anta, A Pérez-Rodríguez, J Castro, C A García- Domínguez, S Ibiza, N Martínez, L M Durá, S Hernández, T Gragera, D Peña-Jiménez, M Yunta, N Zarich, P Crespo, J M Serrador, E Santos, A Muñoz, J L Oliva, J M Rojas-Cabañeros

ABSTRACT

The cyclopentenone prostaglandin A1 (PGA1) is an inducer of cell death in cancer cells. However, the mechanism that initiates this cytotoxic response remains elusive. Here we report that PGA1 triggers apoptosis by a process that entails the specific activation of H- and N-Ras isoforms, leading to caspase activation. Cells without H- and N-Ras did not undergo apoptosis upon PGA1 treatment; in these cells, the cellular demise was rescued by overexpression of either H-Ras or N-Ras. Consistently, the mutant H-Ras-C118S, defective for binding PGA1, did not produce cell death. Molecular analysis revealed a key role for the RAF-MEK-ERK signaling pathway in the apoptotic process through the induction of calpain activity and caspase-12 cleavage. We propose that PGA1 evokes a specific physiological cell death program, through H- and N-Ras, but not K-Ras, activation at endomembranes. Our results highlight a novel mechanism that may be of potential interest for tumor treatment. More... »

PAGES

e2311-e2311

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/cddis.2016.219

DOI

http://dx.doi.org/10.1038/cddis.2016.219

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1010868951

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27468687


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326 rdf:type schema:Organization
327 grid-institutes:grid.465524.4 schema:alternateName Departamento de Biología Celular e Inmunología, Centro de Biología Molecular Severo Ochoa (CBMSO), CSIC-UAM, 28049, Madrid, Spain
328 schema:name Departamento de Biología Celular e Inmunología, Centro de Biología Molecular Severo Ochoa (CBMSO), CSIC-UAM, 28049, Madrid, Spain
329 rdf:type schema:Organization
330 grid-institutes:grid.466793.9 schema:alternateName Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Arturo Duperier 4, 28029, Madrid, Spain
331 schema:name Instituto de Investigaciones Biomédicas ‘Alberto Sols’, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Arturo Duperier 4, 28029, Madrid, Spain
332 rdf:type schema:Organization
333 grid-institutes:grid.507090.b schema:alternateName Departamento de Biologia Molecular, Facultad de Medicina, Instituto de Biomedicina y Biotecnología de Cantabria, Consejo Superior de Investigaciones Cientificas (CSIC)-IDICAN, Universidad de Cantabria, 39011, Santander, Spain
334 schema:name Departamento de Biologia Molecular, Facultad de Medicina, Instituto de Biomedicina y Biotecnología de Cantabria, Consejo Superior de Investigaciones Cientificas (CSIC)-IDICAN, Universidad de Cantabria, 39011, Santander, Spain
335 rdf:type schema:Organization
336 grid-institutes:grid.512888.e schema:alternateName Unidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC), Instituto de Salud Carlos III, 28220, Madrid, Spain
337 schema:name Unidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas (UFIEC), Instituto de Salud Carlos III, 28220, Madrid, Spain
338 rdf:type schema:Organization
339 grid-institutes:grid.9983.b schema:alternateName 8Current address: Immunobiology Unit, Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Lisboa, Portugal.
340 schema:name 8Current address: Immunobiology Unit, Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Lisboa, Portugal.
341 Fundación Centro Nacional de Investigaciones Cardiovasculares (CNIC), 28029, Madrid, Spain
342 rdf:type schema:Organization
 




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