Implications of Therapy-Induced Selective Autophagy on Tumor Metabolism and Survival

Accumulating evidence indicates that therapies designed to trigger apoptosis in tumor cells cause mitochondrial depolarization, nuclear damage, and the accumulation of misfolded protein aggregates, resulting in the activation of selective forms of autophagy. These selective forms of autophagy, inclu...

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Main Authors: Luke R. K. Hughson, Vincent I. Poon, Jaeline E. Spowart, Julian J. Lum
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:International Journal of Cell Biology
Online Access:http://dx.doi.org/10.1155/2012/872091
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author Luke R. K. Hughson
Vincent I. Poon
Jaeline E. Spowart
Julian J. Lum
author_facet Luke R. K. Hughson
Vincent I. Poon
Jaeline E. Spowart
Julian J. Lum
author_sort Luke R. K. Hughson
collection DOAJ
description Accumulating evidence indicates that therapies designed to trigger apoptosis in tumor cells cause mitochondrial depolarization, nuclear damage, and the accumulation of misfolded protein aggregates, resulting in the activation of selective forms of autophagy. These selective forms of autophagy, including mitophagy, nucleophagy, and ubiquitin-mediated autophagy, counteract apoptotic signals by removing damaged cellular structures and by reprogramming cellular energy metabolism to cope with therapeutic stress. As a result, the efficacies of numerous current cancer therapies may be improved by combining them with adjuvant treatments that exploit or disrupt key metabolic processes induced by selective forms of autophagy. Targeting these metabolic irregularities represents a promising approach to improve clinical responsiveness to cancer treatments given the inherently elevated metabolic demands of many tumor types. To what extent anticancer treatments promote selective forms of autophagy and the degree to which they influence metabolism are currently under intense scrutiny. Understanding how the activation of selective forms of autophagy influences cellular metabolism and survival provides an opportunity to target metabolic irregularities induced by these pathways as a means of augmenting current approaches for treating cancer.
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spelling doaj-art-180367eaef8f46cc8279934c7f0ee30b2025-02-03T06:07:00ZengWileyInternational Journal of Cell Biology1687-88761687-88842012-01-01201210.1155/2012/872091872091Implications of Therapy-Induced Selective Autophagy on Tumor Metabolism and SurvivalLuke R. K. Hughson0Vincent I. Poon1Jaeline E. Spowart2Julian J. Lum3Deeley Research Centre, BC Cancer Agency, 2410 Lee Avenue, Victoria, BC, V8R 6V5, CanadaDeeley Research Centre, BC Cancer Agency, 2410 Lee Avenue, Victoria, BC, V8R 6V5, CanadaDeeley Research Centre, BC Cancer Agency, 2410 Lee Avenue, Victoria, BC, V8R 6V5, CanadaDeeley Research Centre, BC Cancer Agency, 2410 Lee Avenue, Victoria, BC, V8R 6V5, CanadaAccumulating evidence indicates that therapies designed to trigger apoptosis in tumor cells cause mitochondrial depolarization, nuclear damage, and the accumulation of misfolded protein aggregates, resulting in the activation of selective forms of autophagy. These selective forms of autophagy, including mitophagy, nucleophagy, and ubiquitin-mediated autophagy, counteract apoptotic signals by removing damaged cellular structures and by reprogramming cellular energy metabolism to cope with therapeutic stress. As a result, the efficacies of numerous current cancer therapies may be improved by combining them with adjuvant treatments that exploit or disrupt key metabolic processes induced by selective forms of autophagy. Targeting these metabolic irregularities represents a promising approach to improve clinical responsiveness to cancer treatments given the inherently elevated metabolic demands of many tumor types. To what extent anticancer treatments promote selective forms of autophagy and the degree to which they influence metabolism are currently under intense scrutiny. Understanding how the activation of selective forms of autophagy influences cellular metabolism and survival provides an opportunity to target metabolic irregularities induced by these pathways as a means of augmenting current approaches for treating cancer.http://dx.doi.org/10.1155/2012/872091
spellingShingle Luke R. K. Hughson
Vincent I. Poon
Jaeline E. Spowart
Julian J. Lum
Implications of Therapy-Induced Selective Autophagy on Tumor Metabolism and Survival
International Journal of Cell Biology
title Implications of Therapy-Induced Selective Autophagy on Tumor Metabolism and Survival
title_full Implications of Therapy-Induced Selective Autophagy on Tumor Metabolism and Survival
title_fullStr Implications of Therapy-Induced Selective Autophagy on Tumor Metabolism and Survival
title_full_unstemmed Implications of Therapy-Induced Selective Autophagy on Tumor Metabolism and Survival
title_short Implications of Therapy-Induced Selective Autophagy on Tumor Metabolism and Survival
title_sort implications of therapy induced selective autophagy on tumor metabolism and survival
url http://dx.doi.org/10.1155/2012/872091
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