Anoikis molecular pathways and its role in cancer progression.

By P. Paoli, E. Giannoni, P. Chiarugi. Biochimica et Biophysica Acta, 2013

1,094 citations recorded by the source corpus.

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.

Subfields: Cell Biology, Immunology and Allergy, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/3df11501311525dd219a010c5f3de000c08e4cd4

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Citations in the corpus

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, positive): “Conversely, in “type II cells” (e.g., hepatocytes, pancreatic β cells, and a majority of cancer cells), in which CASP3 and CASP7 activation is restrained by XIAP [310], extrinsic apoptosis requires the proteolytic cleavage of BID by CASP8 [70, 311, 312].”
Oxidative Stress in Cancer (2020, background): “Cancer cells can use a wide variety of mechanisms to avoid anoikis, including triggering of EMT, integrin switching, growth factor overexpression, activating pro-survival signaling, activating oncogenes, and adapting metabolism to ameliorate stress (Paoli et al., 2013).”
The lipid kinase PI5P4Kβ is an intracellular GTP sensor for metabolism and tumorigenesis (2016, neutral): “Thus, we compared anchorage-independent soft-agar colony formation of WTPI5P4Kb cells to that of PI5P4Kb cells, where cells are exposed to similar nutrient depleted conditions as cancer cells in tissues (Paoli et al., 2013; Schafer et al., 2009).”
The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis (2022, background): “By regulating pro-apoptotic and anti-apoptotic genes, the “integrin switch” enables cells to make use of survival signals through overexpression or structural activation of integrins, and then changes the cell metabolism to prevent MCSCs from losing their nest due to apoptosis [160, 161].”