Advantages and disadvantages of mitochondrial mechanism (mitophagy) for cancer treatment
Department of Genetics and Bioengineering, International Burch University, Sarajevo, Bosnia and Herzegovina.
Review
World Journal of Biology Pharmacy and Health Sciences, 2024, 18(01), 064–072.
Article DOI: 10.30574/wjbphs.2024.18.1.0180
Publication history:
Received on 24February 2024; revised on 02April 2024; accepted on 05April 2024
Abstract:
Mitochondrial organelles are crucial organelles for the energy supply of the whole cell. Also, mitochondria are beneficial for the production of ATP, a byproduct of the stabilization of nutrients in the TCA cycle, and FADH and NADH are reducing equivalents. Defects in mitochondria impair the energy supply, metabolite production, and redox reactions. Also, a crucial point for cell survival is to maintain mitochondrial quality rather than quantity. Qualitative mitochondria are required to produce the proper amount of ATP, degrade p53, and decrease reactive oxygen species (ROS) production. All of these factors lead to mitochondrial dysfunction. Dysfunctional mitochondria are „eaten“ by autophagosomes through the process of mitophagy. Mitophagy is crucial since it prevents the build-up of poorly/affected mitochondria, and prevents excess production of ROS and mtDNA mutation. Also, mitophagy shows positive effects on cancer, since mitophagy promotes pro-apoptotic signals for cancer stem cells (CSC). Due to all the advantages of mitophagy, this organelle can be used as a beneficial assistant for chemotherapy in cancer treatment. The authors of these papers provide a pathway for using mitophagy combined with cancer treatment. This claim is confirmed within the paper, with tables provided. Our results show the importance of mitophagy in human organisms and its importance in cancer.
Keywords:
Mitochondria; Mitophagy; Cancer; Mitochondrial dysfunction; Chemotherapy
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Copyright © 2024 Author(s) retain the copyright of this article. This article is published under the terms of the Creative Commons Attribution Liscense 4.0