Mitochondrial apoptosis: killing cancer using the enemy within
By Jonathan Lopez, S. Tait. British Journal of Cancer, 2015
686 citations recorded by the source corpus.
Apoptotic cell death inhibits oncogenesis at multiple stages, ranging from transformation to metastasis. Consequently, in order for cancer to develop and progress, apoptosis must be inhibited. Cell death also plays major roles in cancer treatment, serving as the main effector function of many anti-cancer therapies. In this review, we discuss the role of apoptosis in the development and treatment of cancer. Specifically, we focus upon the mitochondrial pathway of apoptosis—the most commonly deregulated form of cell death in cancer. In this process, mitochondrial outer membrane permeabilisation or MOMP represents the defining event that irrevocably commits a cell to die. We provide an overview of how this pathway is regulated by BCL-2 family proteins and describe ways in which cancer cells can block it. Finally, we discuss exciting new approaches aimed at specifically inducing mitochondrial apoptosis in cancer cells, outlining their potential pitfalls, while highlighting their considerable therapeutic promise.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/0c3a02859f0609693239a989ae86129adaaa1061
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In Molecular Biology
Citations in the corpus
- Revisiting the hallmarks of cancer. (2017, neutral): “Cancer cells are able to surpass apoptotic response by various mechanisms [51, 53].”
- Flavonoids in Cancer and Apoptosis (2018, background): “p53 is also associated with lysosomal permeabilization, releasing cathepsin that activates Bid and Bak on the mitochondrial membrane [14,15].”
- Apoptosis: A Target for Anticancer Therapy (2018, background): “The intrinsic pathway, in particular, is regulated by the B-cell lymphoma-2 (BCL-2) protein family which include proapoptotic effector proteins, proapoptotic BH3-only proteins, and antiapoptotic BCL-2 proteins [3].”