The Mechanisms of Mitochondria-Mediated Apoptosis in Cancer Chemotherapy
Cell Biology
Volume 3, Issue 2-1, April 2015, Pages: 17-21
Received: Feb. 3, 2015; Accepted: Feb. 27, 2015; Published: Mar. 12, 2015
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Author
Ashutosh Shrivastava, Division of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave, Boston, MA 02115
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Abstract
Cell metabolism and signal transduction has usually been considered independent processes. Interestingly mitochondria is an intracellular organelle that perform energy production to fuel the cell to carry out its normal functions, however, in certain circumstances, its components can also carry out programmed cell destruction via its resident proteins. In this review, the role of mitochondria and its component proteins in inducing apoptotic programmed cell death is discussed. The role of Bcl-2 family proteins that set up the mitochondria induced apoptotic threshold is also described. Further, how the metabolic stress leads to mitochondrial dysfunction via increased generation of reactive oxygen species are discussed. This article is a part of a special issue on mitochondria summarizes the induction of intracellular pathways that converge on mitochondria and ultimately impact the success of chemotherapeutic interventions.
Keywords
Mitochondria, Cancer, Apoptosis, Programmed Cell Death
To cite this article
Ashutosh Shrivastava, The Mechanisms of Mitochondria-Mediated Apoptosis in Cancer Chemotherapy, Cell Biology. Special Issue: Mitochondria: Implications in Human Health and Diseases. Vol. 3, No. 2-1, 2015, pp. 17-21. doi: 10.11648/j.cb.s.2015030201.13
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