Mitochondrial Respiration and Energy Metabolism in Cancer Cells
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".
Deadline for manuscript submissions: 20 March 2025 | Viewed by 660
Special Issue Editor
Special Issue Information
Dear Colleagues,
Mitochondria are intracellular organelles involved in energy production, cell metabolism and cell signaling and consume over 95% of all oxygen that reaches our cells in order to produce ATP through oxidative phosphorylation. Mitochondria are essential not only in the process of energetic ATP synthesis but also in lipid metabolism, amino acid metabolism, the TCA cycle, and nucleic acid metabolism. Mitochondria have their own mitochondrial DNA. Mutations in mtDNA and in the nuclear genes encoding mitochondrial proteins (TCA cycle, respiratory chain complexes) are commonly observed in cancer cells and are involved in cancer metabolism remodeling. Moreover, mitochondria play critical roles in many physiological processes, such as apoptosis and redox or calcium homeostasis and produce large amounts of reactive oxygen species (ROS) that can contribute to oxidative stress and potentially promote cancer development. Dysfunctional mitochondria can lead to metabolic reprogramming in cancer cells, allowing them to meet the increased energy demands associated with rapid proliferation. For energy, cancer cells utilize glycolysis preferentially over mitochondrial oxidative phosphorylation even in aerobic circumstances, also called the Warburg effect. Decreased cellular respiration due to hypoxia and increased ROS could affect cancer cell proliferation. The regulatory mechanisms leading to decreased cellular respiration in cancer cells are complicated and may depend on tumor type.
Prof. Dr. Rasa Banienė
Guest Editor
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Keywords
- mitochondria
- respiration
- cancer
- ATP synthesis
- mtDNA
- oxidative stress
- glycolysis
- cell death
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