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TP53 transcription factor for the NEDD9/HEF1/Cas-L gene: potential targets in Non-Small Cell Lung Cancer treatment.
Rousseau, Bénédicte; Jacquot, Catherine; Le Palabe, Julie; Malleter, Marine; Tomasoni, Christophe; Boutard, Tifenn; Sakanyan, Vehary; Roussakis, Christos.
Afiliación
  • Rousseau B; IICiMED/EA 1155 - Département Cancer du Poumon et Cibles Moléculaires, UFR Sciences Pharmaceutiques - 9 rue Bias - BP53508 - 44035 NANTES CEDEX 1 - FRANCE.
  • Jacquot C; IICiMED/EA 1155 - Département Cancer du Poumon et Cibles Moléculaires, UFR Sciences Pharmaceutiques - 9 rue Bias - BP53508 - 44035 NANTES CEDEX 1 - FRANCE.
  • Le Palabe J; IICiMED/EA 1155 - Département Cancer du Poumon et Cibles Moléculaires, UFR Sciences Pharmaceutiques - 9 rue Bias - BP53508 - 44035 NANTES CEDEX 1 - FRANCE.
  • Malleter M; UMR INSERM U 1085 Groupe "Death receptors and tumor escape" - Université de Rennes 1 Campus Santé - Bâtiment 5 - 2 avenue du Prof Léon Bernard - 35043 RENNES - France.
  • Tomasoni C; IICiMED/EA 1155 - Département Cancer du Poumon et Cibles Moléculaires, UFR Sciences Pharmaceutiques - 9 rue Bias - BP53508 - 44035 NANTES CEDEX 1 - FRANCE.
  • Boutard T; IICiMED/EA 1155 - Département Cancer du Poumon et Cibles Moléculaires, UFR Sciences Pharmaceutiques - 9 rue Bias - BP53508 - 44035 NANTES CEDEX 1 - FRANCE.
  • Sakanyan V; IICiMED/EA 1155 - Département Cancer du Poumon et Cibles Moléculaires, UFR Sciences Pharmaceutiques - 9 rue Bias - BP53508 - 44035 NANTES CEDEX 1 - FRANCE.
  • Roussakis C; IICiMED/EA 1155 - Département Cancer du Poumon et Cibles Moléculaires, UFR Sciences Pharmaceutiques - 9 rue Bias - BP53508-44035 NANTES CEDEX 1-FRANCE.
Sci Rep ; 5: 10356, 2015 May 26.
Article en En | MEDLINE | ID: mdl-26011298
Lung cancer is a serious public health problem. Although there has been significant progress in chemotherapy, non-small cell lung cancer is still resistant to current treatments, primarily because of the slow rate of cell development. It is thus important to find new molecules directed against targets other than proliferation agents. Considering the high proportion of mutant proteins in tumor cells, and the high rate of mutation of the TP53 gene in all cancers, and in NSCLC in particular, this gene is a perfect target. Certain new molecules have been shown to restore the activity of mutated p53 protein, for example PRIMA-1, which reactivates the His273 mutant p53. In a previous study, we presented triazine A190, a molecule with a cytostatic activity that blocks cells in the G1 phase and induces apoptosis. Here, we show that A190 not only restores mutant p53 activity, but also induces an overexpression of the NEDD9 gene, leading to apoptotic death. These findings might offer hope for the development of new targeted therapies, specific to tumor cells, which spare healthy cells.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fosfoproteínas / Proteína p53 Supresora de Tumor / Proteínas Adaptadoras Transductoras de Señales Límite: Humans Idioma: En Revista: Sci Rep Año: 2015 Tipo del documento: Article Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Fosfoproteínas / Proteína p53 Supresora de Tumor / Proteínas Adaptadoras Transductoras de Señales Límite: Humans Idioma: En Revista: Sci Rep Año: 2015 Tipo del documento: Article Pais de publicación: Reino Unido