Anoikis molecular pathways and its role in cancer progression
Open accessAbstract
Anoikis is a programmed cell death induced upon cell detachment from extracellular matrix, behaving as a critical mechanism in preventing adherent-independent cell growth and attachment to an inappropriate matrix, thus avoiding colonizing of distant organs. As anchorage-independent growth and epithelial-mesenchymal transition, two features associated with anoikis resistance, are vital steps during cancer progression and metastatic colonization, the ability of cancer cells to resist anoikis has now attracted main attention from the scientific community. Cancer cells develop anoikis resistance due to several mechanisms, including change in integrins' repertoire allowing them to grow in different niches, activation of a plethora of inside-out pro-survival signals as over-activation of receptors due to sustained autocrine loops, oncogene activation, growth factor receptor overexpression, or mutation/upregulation of key enzymes involved in integrin or growth factor receptor signaling. In addition, tumor microenvironment has also been acknowledged to contribute to anoikis resistance of bystander cancer cells, by modulating matrix stiffness, enhancing oxidative stress, producing pro-survival soluble factors, triggering epithelial-mesenchymal transition and self-renewal ability, as well as leading to metabolic deregulations of cancer cells. All these events help cancer cells to inhibit the apoptosis machinery and sustain pro-survival signals after detachment, counteracting anoikis and constituting promising targets for anti-metastatic pharmacological therapy. This article is part of a Special Section entitled: Cell Death Pathways.
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Anoikis is a specific variant of intrinsic apoptosis elicited by the loss of integrin-dependent attachment to the extracellular matrix.
“A specific variant of intrinsic apoptosis elicited by the loss of integrin-dependent attachment to the extracellular matrix is commonly known as anoikis [233, 234].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [233]
Anoikis is demarcated by MOMP and precipitated by the activation of executioner caspases, notably CASP3.
“As such, anoikis is demarcated by MOMP and precipitated by the activation of executioner caspases, notably CASP3 [233].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [233]
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- Authors
- Paoli, P., Giannoni, E., & Chiarugi, P.
- Affiliations
- University of Florence (IT)
- Tumour Institute of Tuscany (IT)
- Corresponding author
- Chiarugi, Paola
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 1833
- Issue
- 12
- Pages
- 3481-3498
- ISSN
- 0167-4889 (ISSN-L)
- OpenAlex
- W2138362890
- Cited by
- 1,160
- References
- 269
- Citations by year
- 2026: 52 · 2025: 98 · 2024: 120 · 2023: 117 · 2022: 122 · 2021: 123 · 2020: 109 · 2019: 87 · 2018: 90 · 2017: 81 · 2016: 77 · 2015: 49 · 2014: 31 · 2013: 2 · 2012: 1
- FWCI
- 4.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Cell Research (publishedVersion)
- PubMed (publishedVersion)
- Florence Research (University of Florence) (submittedVersion)
- Funders
- Associazione Italiana Ricerca sul Cancro (AIRC)
- Istituto Toscano Tumori
- Regione Toscana
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- anoikis, anoikis resistance, tumor progression, metastasis, anchorage-independent growth, epithelial-mesenchymal transition, integrins, inside-out signaling, autocrine loop, oncogene activation, tumor microenvironment, extracellular matrix stiffness, oxidative stress, cancer metabolism, apoptosis, anti-metastatic therapy
- MeSH terms
- Animals, Humans, Neoplasm Metastasis, Neoplasms, Signal Transduction, Disease Progression, Cytoprotection, Anoikis
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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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