Novel Insights into PML-Dependent Oncosuppression.
At odds with its nuclear counterpart, extranuclear promyelocytic leukemia constitutively inhibits autophagy, hence limiting cancer progression. These data raise the interesting possibility that some tumor suppressors have become specialized to operate at multiple subcellular compartments for counteracting different aspects of the oncogenic process.
Department of Radiation Oncology, Weill Cornell Medical College, New York, NY 10065, USA; Equipe 11 Labellisée Ligue Contre le Cancer, Centre de Recherche des Cordeliers, 75006 Paris, France; INSERM, U1138, 75006 Paris, France; Université Paris Descartes/Paris V, Sorbonne Paris Cité, 75006 Paris, France; Université Pierre et Marie Curie/Paris VI, 75006 Paris, France; Gustave Roussy Comprehensive Cancer Institute, 94805 Villejuif, France. Electronic address: deadoc@vodafone.it.
Lorenzo
L
Galluzzi
D000818:Animals; D016147:Genes, Tumor Suppressor; D006801:Humans; D051379:Mice; D008954:Models, Biological; D000071156:Promyelocytic Leukemia Protein / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
D000071156:Promyelocytic Leukemia Protein; D016159:Tumor Suppressor Protein p53
MAMs; autophagy; beclin 1; chloroquine; p53; regulated cell death