2024-03-28T16:01:25Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/386662016-06-18T00:49:21Zcom_10261_134com_10261_1col_10261_387
http://hdl.handle.net/10261/38666
10.1016/j.canlet.2009.06.012
39771
Down-regulation of RIP expression by 17-dimethylaminoethylamino-17-demethoxygeldanamycin promotes TRAIL-induced apoptosis in breast tumor cells
Elsevier
2010
artículo
Palacios, Carmen
López-Pérez, Ana Isabel
López-Rivas, Abelardo
17DMAG
TRAIL
Apoptosis
RIP1
2010-01
9 páginas, 4 figuras.
The Hsp90 inhibitor 17DMAG (17-dimethylaminoethylamino-17-demethoxygeldanamycin) is undergoing clinical trials as an antitumor drug. We show here that treatment of human breast cancer cells with 17DMAG facilitates tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Down-regulation of receptor interacting protein (RIP1) is observed upon 17DMAG treatment concomitantly with inhibition of IκBα phosphorylation. Interestingly, RNAi-mediated knockdown of RIP1 expression is sufficient to sensitize human breast tumor cells to TRAIL-induced apoptosis through a NF-κB-independent, mitochondria-operated pathway. Our results indicate that RIP1 is important in maintaining resistance to TRAIL-induced apoptosis in breast tumor cells and highlight the potential therapeutic benefit of the combination of Hsp90 inhibitors and TRAIL against breast tumor cells.
Ministerio de Educación y Ciencia (España)
Junta de Andalucía
Red Temática de Investigación Cooperativa en Cáncer (España)
Ministerio de Ciencia e Innovación (España)
Cancer Letters
2010
287
207
215