R-RAS2 overexpression in tumors of the human central nervous system
Entidad
UAM. Departamento de Biología MolecularEditor
BioMed CentralFecha de edición
2013-10-23Cita
10.1186/1476-4598-12-127
Molecular Cancer 12.1 (2013): 127
ISSN
1476-4598DOI
10.1186/1476-4598-12-127Financiado por
This work was supported by grants SAF2012-31279 from the ‘Comisión Interministerial de Ciencia y Tecnología’ and the ‘Ramón y Cajal’ program (RYC-2010-06251, to B.C.). We also thank the Fundación Ramón Areces for its institutional support of the ‘Centro de Biología Molecular Severo Ochoa’.Proyecto
Comunidad de Madrid. S2010/BMD-2332/INDISNETVersión del editor
http://dx.doi.org/10.1186/1476-4598-12-127Materias
RAS family proteins; R-RAS2; CNS tumors; TC21; Biología y Biomedicina / BiologíaDerechos
© 2013 Gutierrez-Erlandsson et al.Resumen
Malignant tumors of the central nervous system (CNS) are the 10th most frequent cause of cancer mortality. Despite
the strong malignancy of some such tumors, oncogenic mutations are rarely found in classic members of the RAS
family of small GTPases. This raises the question as to whether other RAS family members may be affected in CNS
tumors, excessively activating RAS pathways. The RAS-related subfamily of GTPases is that which is most closely
related to classical Ras and it currently contains 3 members: RRAS, RRAS2 and RRAS3. While R-RAS and R-RAS2 are
expressed ubiquitously, R-RAS3 expression is restricted to the CNS. Significantly, both wild type and mutated RRAS2
(also known as TC21) are overexpressed in human carcinomas of the oral cavity, esophagus, stomach, skin and
breast, as well as in lymphomas. Hence, we analyzed the expression of R-RAS2 mRNA and protein in a wide variety
of human CNS tumors and we found the R-RAS2 protein to be overexpressed in all of the 90 CNS cancer samples
studied, including glioblastomas, astrocytomas and oligodendrogliomas. However, R-Ras2 was more strongly
expressed in low grade (World Health Organization grades I-II) rather than high grade (grades III-IV) tumors,
suggesting that R-RAS2 is overexpressed in the early stages of malignancy. Indeed, R-RAS2 overexpression was
evident in pre-malignant hyperplasias, both at the mRNA and protein levels. Nevertheless, such dramatic changes in
expression were not evident for the other two subfamily members, which implies that RRAS2 is the main factor
triggering neural transformation.
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Google Scholar:Gutiérrez-Erlandsson, Sylvia
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Herrero-Vidal, Pedro
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Fernández-Alfara, Marcos
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Hernández-García, Susana
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Gonzalo-Flores, Sandra
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Mudarra-Rubio, Alberto
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Fresno Escudero, Manuel
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Cubelos Álvarez, Beatriz
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