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Título: | p38α limits the contribution of MAP17 to cancer progression in breast tumors |
Autor: | Guijarro, M. V.; Vergel, Mar CSIC; Marín, Juan J. CSIC; Muñoz-Galván, Sandra CSIC ORCID ; Ferrer, Irene; Ramón y Cajal, Santiago; Roncador, Giovanna; Blanco-Aparicio, Carmen; Carnero, Amancio CSIC ORCID | Palabras clave: | ROS Breast carcinoma MAP17 p38 |
Fecha de publicación: | 11-oct-2012 | Editor: | Springer Nature | Citación: | Oncogene 31: 4447-4459 (2012) | Resumen: | MAP17 is a small, 17-kDa, non-glycosylated membrane protein that is overexpressed in a percentage of carcinomas. In the present work, we have analyzed the role of MAP17 expression during mammary cancer progression. We have found that MAP17 is expressed in 60% human mammary tumors while it is not expressed in normal or benign neoplasias. MAP17 levels increased with breast tumor stage and were strongly correlated with mammary tumoral progression. A significant increase in the levels of reactive oxygen species (ROS) was observed in MAP17-expressing cells, as compared with parental cells. This increase was further paralleled by an increase in the tumorigenic capacity of carcinoma cells but not in immortal non-tumoral breast epithelial cells, which provides a selective advantage once tumorigenesis has begun. Expression of specific MAP17 shRNA in protein-expressing tumor cells reduced their tumorigenic capabilities, which suggests that this effect is dependent upon MAP17 protein expression. Our data show that ROS functions as a second messenger that enhances tumoral properties, which are inhibited in non-tumoral cells. We have found that p38α activation mediates this response. MAP17 triggers a ROS-dependent, senescence-like response that is abolished in the absence of p38a activation. Furthermore, in human breast tumors, MAP17 activation is correlated with a lack of phosphorylation of p38α. Therefore, MAP17 is overexpressed in late-stage breast tumors, in which oncogenic activity relies on p38 insensitivity to induce intracellular ROS. | Versión del editor: | https://doi.org/10.1038/onc.2011.619 | URI: | http://hdl.handle.net/10261/345313 | DOI: | 10.1038/onc.2011.619 | ISSN: | 0950-9232 | E-ISSN: | 1476-5594 |
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