Mitocans Revisited: Mitochondrial Targeting as Efficient Anti-Cancer Therapy.

Abstract

Mitochondria are essential cellular organelles, controlling multiple signalling pathways critical for cell survival and cell death. Increasing evidence suggests that mitochondrial metabolism and functions are indispensable in tumorigenesis and cancer progression, rendering mitochondria and mitochondrial functions as plausible targets for anti-cancer therapeutics. In this review, we summarised the major strategies of selective targeting of mitochondria and their functions to combat cancer, including targeting mitochondrial metabolism, the electron transport chain and tricarboxylic acid cycle, mitochondrial redox signalling pathways, and ROS homeostasis. We highlight that delivering anti-cancer drugs into mitochondria exhibits enormous potential for future cancer therapeutic strategies, with a great advantage of potentially overcoming drug resistance. Mitocans, exemplified by mitochondrially targeted vitamin E succinate and tamoxifen (MitoTam), selectively target cancer cell mitochondria and efficiently kill multiple types of cancer cells by disrupting mitochondrial function, with MitoTam currently undergoing a clinical trial.

• Authors: Lanfeng Dong, Vinod Gopalan, Olivia Holland, Jiri Neuzil
• Journal: International journal of molecular sciences (Int J Mol Sci) Vol. 21 Issue 21 (Oct 26 2020) ISSN: 1422-0067 [Electronic] Switzerland
• PMID: 33114695 (Publication Type: Journal Article, Review)

Chemical References

• Antineoplastic Agents
• Electron Transport Chain Complex Proteins

Topics

• Antineoplastic Agents (pharmacology, therapeutic use)
• Citric Acid Cycle (drug effects)
• Clinical Trials as Topic
• Disease Progression
• Drug Resistance, Neoplasm (drug effects)
• Electron Transport Chain Complex Proteins (drug effects, metabolism)
• Gene Expression Regulation, Neoplastic (drug effects)
• Humans
• Mitochondria (drug effects, metabolism)
• Molecular Targeted Therapy
• Neoplasms (drug therapy, metabolism)
• Oxidation-Reduction (drug effects)
• Signal Transduction (drug effects)