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• W2009850885 abstract "The endoplasmic reticulum (ER) has recently emerged as an alternative target to induce cell death in tumours, since prolonged ER stress results in the induction of apoptosis also in chemoresistant transformed cells. Here we show the DNA damage-upregulated/activated pro-apoptotic factor E2F1 is unexpectedly down-regulated during the ER stress-mediated apoptotic program. E2F1 decline is a late event during the ER response mediated by the two UPR sensors and key players ATF6 and IRE1. While ATF6 directly interacts with E2F1 promoter, IRE1 requires the involvement of the known E2F1 modulator E2F7, through the activation of its main target Xbp-1. Importantly, inhibition of E2F1 decrease prevents ER stress-induced apoptosis, while E2F1 knock-down efficiently sensitize cells to ER stress-dependent apoptosis leading to the up-regulation of two main factors in the UPR pro-apoptotic execution phase, Puma and Noxa. Our results point out a novel key role of E2F1 in the survival/death cell decision under ER stress, and unveil E2F1 inactivation as a valuable novel potential therapeutic strategy to increase the response of tumour cells to ER stress-based anticancer treatments." @default.
• W2009850885 created "2016-06-24" @default.
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• W2009850885 date "2015-01-01" @default.
• W2009850885 modified "2023-10-18" @default.
• W2009850885 title "Down-regulation of E2F1 during ER stress is required to induce apoptosis" @default.
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• W2009850885 doi "https://doi.org/10.1242/jcs.164103" @default.
• W2009850885 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25616897" @default.
• W2009850885 hasPublicationYear "2015" @default.
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