2024-03-28T09:47:31Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/1242082016-02-18T03:22:16Zcom_10261_134com_10261_1col_10261_513
http://hdl.handle.net/10261/124208
303159
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
2013
póster de congreso
Martín-Pérez, Rosa
Palacios, Carmen
Yerbes, Rosario
Cano-González, Ana
López-Rivas, Abelardo
2013-10-08
Póster presentado en Cold Spring Harbor Meeting on Cell Death, celebrado en New York (USA) del 8 al 12 de octubre de 2013
Cancer 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
Cold Spring Harbor Meeting on Cell Death