The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
PERK promotes cancer cell proliferation and tumor growth by limiting oxidative DNA damage
Open accessAbstract
To proliferate and expand in an environment with limited nutrients, cancer cells co-opt cellular regulatory pathways that facilitate adaptation and thereby maintain tumor growth and survival potential. The endoplasmic reticulum (ER) is uniquely positioned to sense nutrient deprivation stress and subsequently engage signaling pathways that promote adaptive strategies. As such, components of the ER stress-signaling pathway represent potential antineoplastic targets. However, recent investigations into the role of the ER resident protein kinase, RNA-dependent protein kinase (PKR)-like ER kinase (PERK) have paradoxically suggested both pro- and anti-tumorigenic properties. We have used animal models of mammary carcinoma to interrogate the contribution of PERK in the neoplastic process. The ablation of PERK in tumor cells resulted in impaired regeneration of intracellular antioxidants and accumulation of reactive oxygen species triggering oxidative DNA damage. Ultimately, PERK deficiency impeded progression through the cell cycle because of the activation of the DNA damage checkpoint. Our data reveal that PERK-dependent signaling is used during both tumor initiation and expansion to maintain redox homeostasis, thereby facilitating tumor growth.
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Cited by
The integrated stress response: From mechanism to disease
Costa-Mattioli, M., & Walter, P. (2020) · Science · doi:10.1126/science.aat5314 · Cited by 1,617
The Molecular Mechanisms Regulating the KEAP1-NRF2 Pathway
Baird, L., & Yamamoto, M. (2020) · Molecular and Cellular Biology · doi:10.1128/mcb.00099-20 · Cited by 1,542
Endoplasmic reticulum stress signals in the tumour and its microenvironment
Chen, X., & Cubillos-Ruiz, J. R. (2021) · Nature Reviews Cancer · doi:10.1038/s41568-020-00312-2 · Cited by 1,356
PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress
Verfaillie, T., Rubio, N., Garg, A. D., Bultynck, G., Rizzuto, R., Decuypere, J.-P., Piette, J., Linehan, C., Gupta, S., Samali, A., et al. (2012) · Cell Death & Differentiation · doi:10.1038/cdd.2012.74 · Cited by 850
Endoplasmic Reticulum Stress and the Hallmarks of Cancer
Urra, H., Dufey, E., Avril, T., Chevet, E., & Hetz, C. (2016) · Trends in Cancer · doi:10.1016/j.trecan.2016.03.007 · Cited by 615
Metadata
- Authors
- Bobrovnikova-Marjon, E., Grigoriadou, C., Pytel, D., Zhang, F., Ye, J., Koumenis, C., Cavener, D., & Diehl, J. A.
- Venue
- Oncogene
- Published
- 2010-05-10
- Volume
- 29
- Issue
- 27
- Pages
- 3881-3895
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W1979592430
- Cited by
- 300
- References
- 13
- FWCI
- 5.95
- Type
- journal article
- Language
- en
- Open access
- green
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- Bobrovnikova-Marjon, E., Grigoriadou, C., Pytel, D., Zhang, F., Ye, J., Koumenis, C., Cavener, D., & Diehl, J. A. (2010). PERK promotes cancer cell proliferation and tumor growth by limiting oxidative DNA damage. Oncogene. https://doi.org/10.1038/onc.2010.153
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