Apoptosis and Autophagy: Therapeutic Implications in Cancer
DOI:
https://doi.org/10.52756/ijerr.2024.v37spl.004Keywords:
Cell death, Autophagy, Apoptosis, Crosstalk, Cancer, Cellular stress responseAbstract
Despite the advances in the medical field so far, cancer remains a global health priority even now. Considering the drug resistance and the failure of cancer therapies to achieve complete eradication of cancer cells in certain populations, developing molecules that induce programmed cell death or apoptosis has been the focus of cancer research for several decades. Apoptosis evasion is one of the hallmarks of cancer cells, and efforts continue to achieve complete annihilation of cancer cells through selective killing. On the other hand, autophagy, a mode of cell degradation, is considered a double-edged sword. Recent studies show that autophagy also can be manipulated to selectively target cancer cells based on the tumor microenvironment and cellular context. Studies show that autophagy is an evolutionarily conserved process initiated during stress response and has enormous importance in maintaining physiological balance. Most importantly, the dynamic equilibrium between apoptosis and autophagy is crucial in maintaining cellular homeostasis. Although a ‘cell eating’ process, the fate of autophagic cells depends entirely on the nature of stress and the extent of crosstalk between autophagy. This understanding is of immense significance when designing therapeutic interventions targeting apoptosis and autophagy. Currently, several studies are ongoing to gain insights into the role of autophagy in cancer initiation, invasion, progression, angiogenesis, and metastasis. This review focuses on the two major cell death mechanisms, apoptosis and autophagy, in the context of cancer, their crosstalk, and the therapeutic interventions targeting both modes of cell death.
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El-Khoury, V., Pierson, S., Szwarcbart, E., Brons, N. H. C., Roland, O., Cherrier-De Wilde, S., Plawny, L., Van Dyck, E., & Berchem, G. (2014). Disruption of autophagy by the histone deacetylase inhibitor MGCD0103 and its therapeutic implication in B-cell chronic lymphocytic leukemia. Leukemia, 28(8), 1636–1646. https://doi.org/10.1038/leu.2014.19
Fairlie, W. D., Tran, S., & Lee, E. F. (2020). Chapter Four—Crosstalk between apoptosis and autophagy signaling pathways. In J. K. E. Spetz & L. Galluzzi (Eds.), International Review of Cell and Molecular Biology (Vol. 352, pp. 115–158). Academic Press. https://doi.org/10.1016/bs.ircmb.2020.01.003
Filomeni, G., De Zio, D., & Cecconi, F. (2015). Oxidative stress and autophagy: The clash between damage and metabolic needs. Cell Death & Differentiation, 22(3), Article 3. https://doi.org/10.1038/cdd.2014.150
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Di Filippo, M., & Bernardi, G. (2009). The Early Apoptotic DNA Fragmentation Targets a Small Number of Specific Open Chromatin Regions. PLoS ONE, 4(4), e5010. https://doi.org/10.1371/journal.pone.0005010
Di Malta, C., Cinque, L., & Settembre, C. (2019). Transcriptional Regulation of Autophagy: Mechanisms and Diseases. Frontiers in Cell and Developmental Biology, 7.
https://www.frontiersin.org/articles/10.3389/fcell.2019.00114
Di Nardo, A., Wertz, M. H., Kwiatkowski, E., Tsai, P. T., Leech, J. D., Greene-Colozzi, E., Goto, J., Dilsiz, P., Talos, D. M., Clish, C. B., Kwiatkowski, D. J., & Sahin, M. (2014). Neuronal Tsc1/2 complex controls autophagy through AMPK-dependent regulation of ULK1. Human Molecular Genetics, 23(14), 3865–3874. https://doi.org/10.1093/hmg/ddu101
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