Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy
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...
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| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2010-01-01
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| Series: | International Journal of Cell Biology |
| Online Access: | http://dx.doi.org/10.1155/2010/930509 |
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| _version_ | 1832550091428200448 |
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| author | Tom Verfaillie Maria Salazar Guillermo Velasco Patrizia Agostinis |
| author_facet | Tom Verfaillie Maria Salazar Guillermo Velasco Patrizia Agostinis |
| author_sort | Tom Verfaillie |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-a75b5b49cf12428785c51fd3a70ccd5a |
| institution | Kabale University |
| issn | 1687-8876 1687-8884 |
| language | English |
| publishDate | 2010-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Cell Biology |
| spelling | doaj-art-a75b5b49cf12428785c51fd3a70ccd5a2025-02-03T06:07:48ZengWileyInternational Journal of Cell Biology1687-88761687-88842010-01-01201010.1155/2010/930509930509Linking ER Stress to Autophagy: Potential Implications for Cancer TherapyTom Verfaillie0Maria Salazar1Guillermo Velasco2Patrizia Agostinis3Department of Molecular Cell Biology, Cell Death Research and Therapy Laboratory, Faculty of Medicine, Catholic University of Leuven, 3000 Leuven, BelgiumDepartment of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, SpainDepartment of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, SpainDepartment of Molecular Cell Biology, Cell Death Research and Therapy Laboratory, Faculty of Medicine, Catholic University of Leuven, 3000 Leuven, BelgiumDifferent 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.http://dx.doi.org/10.1155/2010/930509 |
| spellingShingle | Tom Verfaillie Maria Salazar Guillermo Velasco Patrizia Agostinis Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy International Journal of Cell Biology |
| title | Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy |
| title_full | Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy |
| title_fullStr | Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy |
| title_full_unstemmed | Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy |
| title_short | Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy |
| title_sort | linking er stress to autophagy potential implications for cancer therapy |
| url | http://dx.doi.org/10.1155/2010/930509 |
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