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Mitochondrial Functionality Is Regulated by Alkylphospholipids in Human Colon Cancer Cells
Margalida Torrens-Mas1, Alejandro Collado-Solé1, Alberto Sola-Leyva2
1Grupo Multidisciplinar de Oncología Traslacional, Research Institute of Health Sciences (IUNICS), University of Balearic Islands, 07122 Palma de Mallorca, Spain.
Biology
|December 22, 2023
Summary
Alkylphospholipids (APLs) like perifosine disrupt cancer cell mitochondria, increasing reactive oxygen species (ROS) and reducing viability. This study reveals APLs
Area of Science:
- Mitochondrial Biology
- Cancer Cell Metabolism
- Drug Discovery
Background:
- Alkylphospholipids (APLs) are anticancer agents targeting cell membranes, not DNA.
- APLs disrupt cholesterol transport and metabolism.
- The impact of APLs on mitochondrial function remains unclear.
Purpose of the Study:
- To investigate the effects of APLs on mitochondrial function in colorectal cancer cells.
- To analyze mitochondrial parameters, metabolic rewiring, and cell viability after APL treatment.
Main Methods:
- Treatment of HT29 and SW620 colorectal cancer cells with miltefosine and perifosine.
- Analysis of mitochondrial mass, membrane potential, cardiolipin, H2O2 production, OXPHOS complexes, metabolic enzymes, oxygen consumption, apoptosis, and autophagy markers.
Main Results:
- Perifosine increased mitochondrial mass and reactive oxygen species (ROS) production.
- APLs decreased oxidative phosphorylation (OXPHOS) complexes levels.
- Perifosine induced metabolic rewiring, increasing pyruvate dehydrogenase (PDH) and isocitrate dehydrogenase (IDH) while decreasing lactate dehydrogenase (LDH) activity.
Conclusions:
- APLs, particularly perifosine, induce mitochondrial dysfunction in colorectal cancer cells.
- Increased ROS production and altered metabolism contribute to reduced cellular viability.
- APLs show potential as mitochondrial-targeting anticancer agents.
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