Nutrient deprivation, hypoxia, radiotherapy and chemotherapy induce endoplasmic reticulum (ER) stress, which activates the so-called unfolded protein response (UPR). Extensive and acute ER stress directs the UPR towards activation of death-triggering pathways. Cancer cells are selected to resist mild and prolonged ER stress by activating pro-survival UPR. We recently found that drug-resistant tumor cells are simultaneously resistant to ER stress-triggered cell death. It is not known if cancer cells adapted to ER stressing conditions acquire a chemoresistant phenotype.

PERK induces resistance to cell death elicited by endoplasmic reticulum stress and chemotherapy

SALAROGLIO, IRIS CHIARA;PANADA, ELISA;MOISO, ENRICO;BUONDONNO, ILARIA;PROVERO, Paolo;KOPECKA, JOANNA
Co-last
;
RIGANTI, Chiara
Co-last
2017-01-01

Abstract

Nutrient deprivation, hypoxia, radiotherapy and chemotherapy induce endoplasmic reticulum (ER) stress, which activates the so-called unfolded protein response (UPR). Extensive and acute ER stress directs the UPR towards activation of death-triggering pathways. Cancer cells are selected to resist mild and prolonged ER stress by activating pro-survival UPR. We recently found that drug-resistant tumor cells are simultaneously resistant to ER stress-triggered cell death. It is not known if cancer cells adapted to ER stressing conditions acquire a chemoresistant phenotype.
2017
16
1
91
103
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5427528/
Chemoresistance; Endoplasmic reticulum stress; Eukaryotic translation initiation factor-2α kinase 3/protein kinase RNA-like endoplasmic reticulum kinase; Multidrug resistance related protein 1; Unfolded protein response
Salaroglio, Iris C; Panada, Elisa; Moiso, Enrico; Buondonno, Ilaria; Provero, Paolo; Rubinstein, Menachem; Kopecka, Joanna; Riganti, Chiara
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1637315
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