ER stress‐regulated translation increases tolerance to extreme hypoxia and promotes tumor growth

By M. Bi, Christine Naczki, M. Koritzinsky, Diane R. Fels, Jaime D. Blais, Nianping Hu, H. Harding, I. Novoa, M. Varia, James R. Raleigh and 6 more. EMBO Journal, 2005

777 citations recorded by the source corpus.

Subfields: Cancer Research, Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/7b57860faefdbf76e6dbff88d826378dcadd6d53

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Citations in the corpus

The Cystine/Glutamate Antiporter System xc − in Health and Disease: From Molecular Mechanisms to Novel Therapeutic Opportunities (2013, neutral): “The other candidate nuclear factor that regulates xCT expression is ATF4, which has been reported to be up-regulated in various cancers (25), and its expression level is associated with chemoresistance in cancer cell lines (96).”
Targeting hypoxia in cancer therapy (2011, background): “Gene knockout and RNA interference studies have demonstrated that the PERK–eIF2A–ATF4 and IRE1–XBP1 pathways contribute to hypoxic cell surviva”
Pharmacological brake-release of mRNA translation enhances cognitive memory (2013, background): “During tumor growth, hypoxic conditions and a lack of nutrients can activate both PERK and GCN2, and PERK−/− or GCN2−/− MEFs give rise to significantly smaller tumors in mouse xenograft models than their wild-type counterparts (Bi et al., 2005; Ye et al., 2010).”
The GCN2‐ATF4 pathway is critical for tumour cell survival and proliferation in response to nutrient deprivation (2010, background): “We showed earlier that deficiency in PERK or eIF2a phosphorylation results in decreased resistance to hypoxic stress both in vitro and in vivo (Koumenis et al, 2002; Bi et al, 2005).”
Endoplasmic Reticulum Stress and Oxidative Stress in Cell Fate Decision and Human Disease (2014, background): “The importance of PERK in tumorigenesis is supported by the findings that loss of PERK in mouse fibroblasts and human colon cancer cells reduced tumor growth and angiogenesis when grafted into immunodeficient mice (10, 11).”
Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities (2008, background): “Supporting this notion, GRP78-deficient fibrosarcoma cells as well as XBP1-deficient and PERK-deficient transformed mouse fibroblasts were reported to have significantly reduced tumorigenic activity in mic”
Connecting endoplasmic reticulum stress to autophagy by unfolded protein response and calcium (2007, neutral): “In addition to ER stress, hypoxia also activates the PERKeIF2a-ATF4 and AMPK-mTORC1 pathways.(45,46) It is still unknown whether hypoxia also triggers autophagy, if so the”
Tumorigenic and Immunosuppressive Effects of Endoplasmic Reticulum Stress in Cancer (2017, positive): “PERK-mediated NRF2 stabilization, glutathione synthesis, and HO-1 upregulation collectively reduce cytotoxic ROS levels to facilitate cancer cell growth in vitro and in vivo (Bi et al., 2005; Dey et al., 2015; Rouschop et al., 2013).”
Regulation of cancer cell metabolism (2011, background): “02% O 2 ) causes endoplasmic reticulum stress and activates the unfolded protein response, which provides a further adaptive mechanism that allows tumour cells to survive under adverse metabolic condition”
ER stress: Autophagy induction, inhibition and selection (2015, background): “Hypoxia stimulates extensive downregulation of protein synthesis through activation of the EIF2AK3-EIF2S1-ATF4 and AMPK-MTORC1 pathways.(158,159) Likewise, autophagy can also be triggered under hypoxic conditions, which can be attributed to hypoxia-induced Ca2C influx and activation of CAMK1 (calciu”
The unfolded protein response protects human tumor cells during hypoxia through regulation of the autophagy genes MAP1LC3B and ATG5. (2010, background): “Hypoxic activation of PERK is important because PERK-knockout mouse embryonic fibroblasts (MEFs) or MEFs with a knockin eIF2α mutant allele containing a serine to alanine mutation at position 51 (S51A) show increased cell death during hypoxia and produce slowgrowing tumors with reduced regions of vi”