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http://hdl.handle.net/10261/81518
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dc.contributor.author | Chattopadhyay, S. | - |
dc.contributor.author | Machado-Pinilla, R. | - |
dc.contributor.author | Manguan-García, Cristina | - |
dc.contributor.author | Belda-Iniesta, Cristobal | - |
dc.contributor.author | Moratilla, Carmen | - |
dc.contributor.author | Fresno Vara, Juan Ángel | - |
dc.contributor.author | Castro Carpeño, Javier de | - |
dc.contributor.author | Casado, Enrique | - |
dc.contributor.author | Nistal, Manuel | - |
dc.contributor.author | González Barón, Manuel | - |
dc.contributor.author | Perona Abellón, Rosario | - |
dc.date.accessioned | 2013-09-05T11:03:24Z | - |
dc.date.available | 2013-09-05T11:03:24Z | - |
dc.date.issued | 2006 | - |
dc.identifier | doi: 10.1038/sj.onc.1209364 | - |
dc.identifier | issn: 0950-9232 | - |
dc.identifier | e-issn: 1476-5594 | - |
dc.identifier.citation | Oncogene 25(23): 3335-3345 (2006) | - |
dc.identifier.uri | http://hdl.handle.net/10261/81518 | - |
dc.description.abstract | Non-small-cell lung cancer (NSCLC) represents the most frequent and therapy-refractive sub-class of lung cancer. Improving apoptosis induction in NSCLC represents a logical way forward in treating this tumor. Cisplatin, a commonly used therapeutic agent in NSCLC, induces activation of N-terminal-c-Jun kinase (JNK) that, in turn, mediates induction of apoptosis. In analysing surgical tissue samples of NSCLC, we found that expression of MKP1/CL100, a negative regulator of JNK, showed a strong nuclear staining for tumor cells, whereas, in normal bronchial epithelia, MKP1 was localized in the cytoplasm as well as in nuclei. In the NSCLC-derived cell lines H-460 and H-23, we found that MKP1 was constitutively expressed. Expressing a small-interfering RNA (siRNA) vector for MKP1 in H-460 cells resulted in a more efficient activation by cisplatin of JNK and p38 than in the parental cells, and this correlated with a 10-fold increase in sensitivity to cisplatin. A similar response was also observed in H-460 and H-23 cells when treated with the MKP1 expression inhibitor RO-31-8220. Moreover, expression of a siRNA-MKP2, an MKP1-related phosphatase, had no effect on H-460 cell viability response to cisplatin. Tumors induced by H-460 cells expressing MKP1 siRNA grew slower in nu-/nu- mice and showed more susceptibility to cisplatin than parental cells, and resulted in an impaired growth of the tumor in mice. On the other hand, overexpression of MKP1 in the H-1299 NSCLC-derived cell line resulted in further resistance to cisplatin. Overall, the results showed that inhibition of MKP1 expression contributes to a slow down in cell growth in mice and an increase of cisplatin-induced cell death in NSCLC. As such, MKP1 can be an attractive target in sensitizing cells to cisplatin to increase the effectiveness of the drug in treating NSCLC. © 2006 Nature Publishing Group All rights reserved. | - |
dc.description.sponsorship | This work was supported by the following grants: no. 08.1/0048.1/2003 from the Comunidad Autónoma de Madrid; no. 01/1094, no. 02/0774 and no. 02/1094 from the Fondo de Investigación Sanitaria; no. RTICC C03/10 from Instituto de Salud Carlos III. The investigators RM-P and CM-G are supported by Grant no. RTICC C03/10. | - |
dc.language.iso | eng | - |
dc.publisher | Nature Publishing Group | - |
dc.rights | closedAccess | - |
dc.title | MKP1/CL100 controls tumor growth and sensitivity to cisplatin in non-small-cell lung cancer | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1038/sj.onc.1209364 | - |
dc.date.updated | 2013-09-05T11:03:24Z | - |
dc.description.version | Peer Reviewed | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.openairetype | artículo | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.fulltext | No Fulltext | - |
item.languageiso639-1 | en | - |
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