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Overexpression of the Her2/ERBB2 oncogene in human breast epithelial cells confers sensitivity to endoplasmic reticulum (ER) stress-induced apoptosis by promoting the PERK/ATF4/CHOP and TRAIL-2 pathway dependent activation of caspase-8

AuthorsMartín-Pérez, Rosa ; Palacios, Carmen ; Yerbes, Rosario ; Cano-González, Ana ; López-Rivas, Abelardo
Issue Date8-Oct-2013
CitationCold Spring Harbor Meeting on Cell Death (2013)
AbstractCancer celIs are subject to stressful conditions in theirtumor . . microenviroll1nent, inc1uding low oxygen supply, nument depnvatlOn and pH changes, AlI these stresses activate a range of celIular stress response pafuways, inc1uding the unfolded protem response (UPR) whICh seems to play an important role in tumorigenesis. Our results show fuat human brea~t tumor epithelial celIs that over-express the Her2/ERBB2 oncogene are very sensitive to agents inducing ER stress, To charactenze fue under1ymg mechanism ofthis enhanced sensitivity to ER stress, we have generated a breast epifuelial celIline MCFlOA expressing a constitutive active form of fue oncogen Her2/ERBB2, We have observed fuat expression of fue activated Her2/ERBB2 oncogen confers an increased SenSItlVIty to ER stress agents by promoting fue PERKI ATF4/CHOP pafuway-dependent activation of caspase-8. FinalIy, our results revea! fuat deregulatlOn ofthe MAPKlERK and PI3K1AKT/mTOR pathways in ERBB2-overexpressmg cells is involved in the differential response ofthe UPR to ER stress agents and the resulting cell death
DescriptionPóster presentado en Cold Spring Harbor Meeting on Cell Death, celebrado en New York (USA) del 8 al 12 de octubre de 2013
Appears in Collections:(CABIMER) Comunicaciones congresos
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