In recent years, mitochondrial metabolism has emerged as a target for cancer therapy,
recognizing mitochondria as a central metabolic organelle required for tumorigenesis1.
Mitochondria represent a highly relevant target in oncology.
Many cancers involve gene mutations that alter the bioenergetic state.
In the late 1930s, Nobel laureate Otto Warburg postulated that cancer cells rely on
aerobic glycolysis2‑4, producing excess lactate even in the presence of oxygen.
This metabolic adaptation may help malignant cells evade apoptosis5 and facilitate survival in hypoxic environments6.
Mitochondrial dysfunction in cancer extends to defects in mitochondrial genomics and biogenesis,
apoptotic signaling, and mitochondrial dynamics.
Mitochondrial fusion is required to maintain the mitochondrial genome, while mitochondrial fission
is essential for eliminating damaged mitochondria. Deficits in fission can lead to the accumulation of dysfunctional mitochondria,
and an imbalance in mitochondrial dynamics may contribute to the loss of mtDNA observed in cancer7.
Profiling mitochondrial function in cancer cells enables better understanding of drug response, resistance mechanisms, and metabolic vulnerabilities.