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Autophagy, cancer stem cells and drug resistance
Open accessAbstract
Autophagy is a cellular survival mechanism that is induced by cancer therapy, among other stresses, and frequently contributes to cancer cell survival during long periods of dormancy and the eventual outgrowth of metastatic disease. Autophagy degrades large cellular structures that, once broken down, contribute to cellular survival through the recycling of their constituent metabolites. However, the extent to which this fuel function of autophagy is key to its role in promoting stemness, dormancy and drug resistance remains to be determined. Other roles for autophagy in determining cell fate more directly through targeted degradation of key transcription factors, such as p53 and FoxO3A, or by enforcing a reversible quiescent growth arrest, are discussed in this review. This review also highlights the need to parse out the roles of different forms of selective autophagy in stemness, CD44 expression and dormancy that, for example, are increasingly being attributed explicitly to mitophagy. The clinical relevance of this work and how an increased understanding of functions of autophagy in stemness, dormancy and drug resistance could be manipulated for increased therapeutic benefit, including eliminating minimal residual disease and preventing metastasis, are discussed. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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Mitophagy Controls the Activities of Tumor Suppressor p53 to Regulate Hepatic Cancer Stem Cells
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FIP200 is required for the cell-autonomous maintenance of fetal hematopoietic stem cells
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Functions of autophagy in the tumor microenvironment and cancer metastasis
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Membrane dynamics in autophagosome biogenesis
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A Unified Approach to Targeting the Lysosome's Degradative and Growth Signaling Roles
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Metabolic reprogramming orchestrates cancer stem cell properties in nasopharyngeal carcinoma
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Autophagy Inhibition Mediates Apoptosis Sensitization in Cancer Therapy by Relieving FOXO3a Turnover
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Autophagy positively regulates the CD44+CD24-/lowbreast cancer stem-like phenotype
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Self-citationSystematic analysis of ribophagy in human cells reveals bystander flux during selective autophagy
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Autophagy Supports Breast Cancer Stem Cell Maintenance by Regulating IL6 Secretion
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Autophagy inhibition overcomes multiple mechanisms of resistance to BRAF inhibition in brain tumors
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Atg5 and Ambra1 differentially modulate neurogenesis in neural stem cells
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Wang, C., Liang, C.-C., Bian, Z. C., Zhu, Y., & Guan, J.-L. (2013) · Nature Neuroscience · doi:10.1038/nn.3365 · Cited by 169 · cited 1×
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Basal Autophagy Decreased During the Differentiation of Human Adult Mesenchymal Stem Cells
Oliver, L., Hue, E. S., Priault, M., & Vallette, F. M. (2012) · Stem Cells and Development · doi:10.1089/scd.2012.0124 · Cited by 147
Malignant Precursor Cells Pre-Exist in Human Breast DCIS and Require Autophagy for Survival
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Autophagic homeostasis is required for the pluripotency of cancer stem cells
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A mammosphere formation RNAi screen reveals that ATG4A promotes a breast cancer stem-like phenotype
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Autophagy mediates survival of pancreatic tumour‐initiating cells in a hypoxic microenvironment
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Time to use a dose of Chloroquine as an adjuvant to anti-cancer chemotherapies
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Anabolism-Associated Mitochondrial Stasis Driving Lymphocyte Differentiation over Self-Renewal
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Autophagy and mTORC1 regulate the stochastic phase of somatic cell reprogramming
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Metadata
- Authors
- Smith, A. G., & Macleod, K. F.
- Venue
- The Journal of Pathology
- Publisher
- Wiley
- Published
- 2019-02-04
- Volume
- 247
- Issue
- 5
- Pages
- 708-718
- ISSN
- 0022-3417 (ISSN-L)
- 1096-9896
- OpenAlex
- W2906427523
- Cited by
- 365
- References
- 140
- FWCI
- 24.20
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
