Journal
EMBO MOLECULAR MEDICINE
Volume 12, Issue 5, Pages -Publisher
WILEY
DOI: 10.15252/emmm.201911845
Keywords
cancer; ER stress; MYC; synthetic lethality; UPR
Categories
Funding
- Talent Introduction Fund, Huazhong University of Science and Technology [3004513124]
- Young Scholar Fund, National Natural Science Foundation of China [81802546]
- Southern Eastern Norway Regional Health Authority [2017043]
- Sanming Project of Medicine in Shenzhen [SZSM201911003]
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The transcription factors of the MYC family play pivotal roles in the initiation and progression of human cancers. High oncogenic level of MYC invades low-affinity sites and enhancer sequences, which subsequently alters the transcriptome, causes metabolic imbalance, and induces stress response. The endoplasmic reticulum (ER) not only plays a central role in maintaining proteostasis, but also contributes to other key biological processes, including Ca2+ metabolism and the synthesis of lipids and glucose. Stress conditions, such as shortage in glucose or oxygen and disruption of Ca2+ homeostasis, may perturb proteostasis and induce the unfolded protein response (UPR), which either restores homeostasis or triggers cell death. Crucial roles of ER stress and UPR signaling have been implicated in various cancers, from oncogenesis to treatment response. Here, we summarize the current knowledge on the interaction between MYC and UPR signaling, and its contribution to cancer development. We also discuss the potential of targeting key UPR signaling nodes as novel synthetic lethal strategies in MYC-driven cancers.
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