Stress Management: Death Receptor Signalling and Cross-Talks with the Unfolded Protein Response in Cancer

被引:11
|
作者
Lafont, Elodie [1 ,2 ]
机构
[1] Univ Rennes, INSERM, U1242, F-35042 Rennes, France
[2] Ctr Lutte Canc Eugene Marquis, F-35042 Rennes, France
关键词
death receptor; ER stress; unfolded protein response; TRAIL-R1; 2; CD95; TNFR1; post-translational modifications; cell death; IRE1; PERK; TUMOR-NECROSIS-FACTOR; ENDOPLASMIC-RETICULUM STRESS; APOPTOSIS-INDUCING LIGAND; NF-KAPPA-B; TRAIL-INDUCED APOPTOSIS; ISOLATED LIMB PERFUSION; SOLUBLE FAS LIGAND; AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME; HUMAN-MELANOMA CELLS; ER-STRESS;
D O I
10.3390/cancers12051113
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Throughout tumour progression, tumour cells are exposed to various intense cellular stress conditions owing to intrinsic and extrinsic cues, to which some cells are remarkably able to adapt. Death Receptor (DR) signalling and the Unfolded Protein Response (UPR) are two stress responses that both regulate a plethora of outcomes, ranging from proliferation, differentiation, migration, cytokine production to the induction of cell death. Both signallings are major modulators of physiological tissue homeostasis and their dysregulation is involved in tumorigenesis and the metastastic process. The molecular determinants of the control between the different cellular outcomes induced by DR signalling and the UPR in tumour cells and their stroma and their consequences on tumorigenesis are starting to be unravelled. Herein, I summarize the main steps of DR signalling in relation to its cellular and pathophysiological roles in cancer. I then highlight how the UPR and DR signalling control common cellular outcomes and also cross-talk, providing potential opportunities to further understand the development of malignancies.
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页数:32
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