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T1 Linking ER Stress to Autophagy: Potential Implications for Cancer Therapy
A1 Verfaillie, Tom
A1 Salazar Roa, María
A1 Velasco Díez, Guillermo
A1 Agostinis, Patrizia
AB 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.
PB John Wiley & Sons
SN 1687-8876
YR 2009
FD 2009-10-19
LK https://hdl.handle.net/20.500.14352/125698
UL https://hdl.handle.net/20.500.14352/125698
LA eng
NO Velasco, G., Verfaillie, T., Salazar, M., & Agostinis, P. (2010). [Rev. of Linking ER stress to autophagy: Potential implications for cancer therapy]. International Journal of Cell Biology. https://doi.org/10.1155/2010/930509
NO The work from the author’s laboratories was supported by Grants to P.A. from the K.U.Leuven (OT49/06), F.W.O Flanderen (G.0661.09), and Interuniversity Attraction Pole (IAP) 6/18 initiated by the Belgian State, Science Policy Office as well as by Grants to G.V. from Spanish Ministry of Education and Science (MEC) (HF2005/0021 and SAF2006/00918), Santander-Complutense (PR34/07- 15856), Comunidad de Madrid (S-SAL/0261/2006), GW Pharmaceuticals, and Schering Plough (473/2008).
NO Katholieke Universiteit Leuven
NO Research Foundation Flanders
NO Belgian Federal Science Policy Office
NO Ministerio de Educación y Ciencia (España)
NO Universidad Complutense de Madrid
NO Banco de Santander
NO Comunidad de Madrid
NO GW Pharmaceuticals
DS Docta Complutense
RD 2 abr 2026