Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies
By G. Pistritto, D. Trisciuoglio, Claudia Ceci, Alessia Garufi, G. D’Orazi. Aging, 2016
1,444 citations recorded by the source corpus.
Apoptosis is a form of programmed cell death that results in the orderly and efficient removal of damaged cells, such as those resulting from DNA damage or during development. Apoptosis can be triggered by signals from within the cell, such as genotoxic stress, or by extrinsic signals, such as the binding of ligands to cell surface death receptors. Deregulation in apoptotic cell death machinery is an hallmark of cancer. Apoptosis alteration is responsible not only for tumor development and progression but also for tumor resistance to therapies. Most anticancer drugs currently used in clinical oncology exploit the intact apoptotic signaling pathways to trigger cancer cell death. Thus, defects in the death pathways may result in drug resistance so limiting the efficacy of therapies. Therefore, a better understanding of the apoptotic cell death signaling pathways may improve the efficacy of cancer therapy and bypass resistance. This review will highlight the role of the fundamental regulators of apoptosis and how their deregulation, including activation of anti-apoptotic factors (i.e., Bcl-2, Bcl-xL, etc) or inactivation of pro-apoptotic factors (i.e., p53 pathway) ends up in cancer cell resistance to therapies. In addition, therapeutic strategies aimed at modulating apoptotic activity are briefly discussed.
Subfields: Molecular Biology, Oncology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/158042ca6e509406e0cb7737ce8d92a9fc2f7839
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Citations in the corpus
- Copper metabolism in cell death and autophagy (2023, background): “For example, BAX (BCL2 associated X apoptosis regulator) and BAK1 (BCL2 antagonist/killer 1) can promote apoptosis though oligomerization at the mitochondrial surface to decrease the mitochondrial membrane potential [79,80].”