Epithelial ovarian cancer is one of the most lethal gynecological malignancies worldwide.
Its development strongly depends on several genetic and environmental factors, with
metabolic components and cellular redox homeostasis alterations playing a significant
a role in its development and disease progression. In this review, we summarize the
contribution of mitochondrial and endoplasmic reticulum (ER) stress in the pathogenesis
of epithelial ovarian cancer along with their role as potential biomarkers and therapeutic
targets, including proteins of glucose metabolism, mitochondrial fission and fusion,
mitophagy, membrane-associated ring-CH-type finger 5 (MARCH5), A-kinase anchoring
proteins (AKAPs), proteins regulating mitochondrial Ca2+ homeostasis, mitochondrial
unfolded protein response (UPRmt) proteins, activating transcription factors (ATFs),
CCAAT enhancer binding protein (C/EBP) homologous protein (CHOP), ‘mitokines’, GRP75,
and GRP78. Although many of these potential targets are in preclinical phase, they
have a high potential to become valuable alternative or additive treatments for epithelial
ovarian cancers.
