Signal integration by JNK and p38 MAPK pathways in cancer development.
Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) family members function in a cell context-specific and cell type-specific manner to integrate signals that affect proliferation, differentiation, survival and migration. Consistent with the importance of these events in tumorigenesis, JNK and p38 MAPK signalling is associated with cancers in humans and mice. Studies in mouse models have been essential to better understand how these MAPKs control cancer development, and these models are expected to provide new strategies for the design of improved therapeutic approaches. In this Review we highlight the recent progress made in defining the functions of the JNK and p38 MAPK pathways in different cancers.
Wagner
Erwin F
EF
Centro Nacional de Investigaciones Oncológicas, C/Melchor Fernández Almagro 3, Madrid 28029, Spain. ewagner@cnio.es
Nebreda
Angel R
AR
D000818:Animals; D017209:Apoptosis; D049109:Cell Proliferation; D004195:Disease Models, Animal; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000502:physiology*; D020935:MAP Kinase Signaling System / Q000502:physiology*; D051379:Mice; D009369:Neoplasms / Q000209:etiology* / Q000473:pathology* / Q000628:therapy; D020239:Receptor Cross-Talk; D048051:p38 Mitogen-Activated Protein Kinases / Q000502:physiology*
D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases