The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
Autophagy and metastasis: another double-edged sword
Open accessAbstract
In order to metastasize, tumor cells must adapt to untoward, stressful microenvironments as they disseminate into the systemic circulation and colonize distant organ sites. Autophagy, a tightly regulated lysosomal self-digestion process that is upregulated during cellular stress, has been demonstrated to suppress primary tumor formation, but how autophagy influences metastasis remains unknown. Autophagy may inhibit metastasis by promoting anti-tumor inflammatory responses or by restricting the expansion of dormant tumor cells into macrometastases. Conversely, self-eating may promote metastasis by enhancing tumor cell fitness in response to environmental stresses, such as anoikis, during metastatic progression. Because autophagy is titratable, it may serve both pro- and anti-metastatic functions depending on the contextual demands placed on tumor cells throughout the metastatic process.
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Cites
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Cited by
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Metadata
- Authors
- Kenific, C. M., Thorburn, A., & Debnath, J.
- Venue
- Current Opinion in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2010-04
- Volume
- 22
- Issue
- 2
- Pages
- 241-245
- ISSN
- 0955-0674 (ISSN-L)
- OpenAlex
- W1996362044
- Cited by
- 311
- References
- 34
- FWCI
- 1.07
- Type
- journal article
- Language
- en
- Open access
- green
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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.
