The DOI matches its Crossref record; 25 of the 25 references it cites were found in a registry or an index.
Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy
Open accessAbstract
Different physiological and pathological conditions can perturb protein folding in the endoplasmic reticulum, leading to a condition known as ER stress. ER stress activates a complex intracellular signal transduction pathway, called unfolded protein response (UPR). The UPR is tailored essentially to reestablish ER homeostasis also through adaptive mechanisms involving the stimulation of autophagy. However, when persistent, ER stress can switch the cytoprotective functions of UPR and autophagy into cell death promoting mechanisms. Recently, a variety of anticancer therapies have been linked to the induction of ER stress in cancer cells, suggesting that strategies devised to stimulate its prodeath function or block its prosurvival function, could be envisaged to improve their tumoricidial action. A better understanding of the molecular mechanisms that determine the final outcome of UPR and autophagy activation by chemotherapeutic agents, will offer new opportunities to improve existing cancer therapies as well as unravel novel targets for cancer treatment.
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Cites
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Unfolded proteins and endoplasmic reticulum stress in neurodegenerative disorders
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ROS-mediated mechanisms of autophagy stimulation and their relevance in cancer therapy
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Self-citationWebster, K. A. (2012) · Future Cardiology · doi:10.2217/fca.12.58 · Cited by 302
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Self-citation
Metadata
- Authors
- Verfaillie, T., Salazar, M., Velasco, G., & Agostinis, P.
- Venue
- International Journal of Cell Biology
- Publisher
- Hindawi Limited
- Published
- 2010
- Volume
- 2010
- Pages
- 1-19
- ISSN
- 1687-8876 (ISSN-L)
- 1687-8884
- OpenAlex
- W1993908556
- Cited by
- 346
- References
- 25
- FWCI
- 11.01
- Type
- journal article
- Language
- en
- Open access
- gold
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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