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Open AccessJournal ArticleDOI

CHOP-dependent regulation of p21/waf1 during ER stress.

TLDR
It is shown that tunicamycin, an antibiotic promoting ER stress, suppresses the expression of p21, a tumor suppressor that induces cell cycle arrest and inhibits apoptosis and is consistent with a CHOP-dependent role for p21 in the shift from the pro-survival to thePro-apoptotic function of UPR.
Abstract
The transcription factor CHOP/GADD153 is induced during the unfolded protein response (UPR) and is associated to the induction of ER stress-related apoptosis. However, how the transition between the pro-survival and the pro-apoptotic role of ER stress is being orchestrated remains poorly understood. Here we show that tunicamycin, an antibiotic promoting ER stress, suppresses the expression of p21, a tumor suppressor that induces cell cycle arrest and inhibits apoptosis. This suppression of p21 levels was independent of p53 that is the major transcriptional regulator of p21, but could be reproduced by forced expression of CHOP. Consistently with these findings, siRNA-mediated inhibition of p21 levels restored the sensitivity of CHOP-deficient cells to tunicamycin. Our findings are consistent with a CHOP-dependent role for p21 in the shift from the pro-survival to the pro-apoptotic function of UPR.

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Journal ArticleDOI

The Role of the PERK/eIF2α/ATF4/CHOP Signaling Pathway in Tumor Progression During Endoplasmic Reticulum Stress.

TL;DR: Advancing molecular insight into the transition of tumor cells from adaptation to apoptosis under hypoxia-induced ER stress may provide answers on how to overcome the limitations of current anti-tumor therapies.
Journal ArticleDOI

Reversible inhibitor of p97, DBeQ, impairs both ubiquitin-dependent and autophagic protein clearance pathways

TL;DR: N2,N4-Dibenzylquinazoline-2,4-diamine (DBeQ) was identified as a selective, potent, reversible, and ATP-competitive p97 inhibitor that blocks multiple processes that have been shown by RNAi to depend on p97, including degradation of ubiquitin fusion degradation and endoplasmic reticulum-associated degradation pathway reporters.
Journal ArticleDOI

Cadmium and cellular signaling cascades: interactions between cell death and survival pathways.

TL;DR: This review critically surveys recent literature to outline major features of death and survival signaling pathways as well as their activation, interactions and cross talk in cells exposed to Cd2+.
Journal ArticleDOI

Safranal induces DNA double-strand breakage and ER-stress-mediated cell death in hepatocellular carcinoma cells.

TL;DR: Gene set enrichment analysis provided consistent findings where UPR is among the top terms of up-regulated genes in response to safranal treatment, indicating proteins involved in ER stress were regulated through safranals treatment to induce UPR in HepG2 cells.
References
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Journal ArticleDOI

WAF1, a potential mediator of p53 tumor suppression

TL;DR: A gene is identified, named WAF1, whose induction was associated with wild-type but not mutant p53 gene expression in a human brain tumor cell line and that could be an important mediator of p53-dependent tumor growth suppression.
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The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin-dependent kinases

TL;DR: In this article, an improved two-hybrid system was employed to isolate human genes encoding Cdk-interacting proteins (Cips) and found that CIP1 is a potent, tight-binding inhibitor of Cdks and can inhibit the phosphorylation of Rb by cyclin A-Cdk2.
Journal ArticleDOI

In vivo activation of the p53 pathway by small-molecule antagonists of MDM2.

TL;DR: In this article, the authors identify potent and selective small-molecule antagonists of MDM2 and confirm their mode of action through the crystal structures of complexes, leading to cell cycle arrest, apoptosis, and growth inhibition of human tumor xenografts.
Journal ArticleDOI

Dynamic interaction of BiP and ER stress transducers in the unfolded-protein response

TL;DR: In this article, the lumenal domains of transmembrane protein kinases (PERK and IRE1) were found to be functionally interchangeable in mediating an ER stress response and that in unstressed cells, both L1 and L2 domains formed a stable complex with the ER chaperone BiP.

Dynamic interaction of BiP and ER stress transducers in the unfolded

TL;DR: It is shown that the lumenal domains of these two proteins are functionally interchangeable in mediating an ER stress response and that, in unstressed cells, both lumenAL domains form a stable complex with the ER chaperone BiP.
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