Ovarian cancer (OC) is the most lethal gynecologic
cancer characterized by an elevated apoptosis resistance that, potentially, leads to chemo-resistance in the recurrent disease. Mitochondrial oxidative phosphorylation was found altered in OC, and mitochondria were proposed as a target for
therapy. Molecular evidence suggests that the deregulation of mitochondrial biogenesis, morphology, dynamics, and apoptosis is involved in
carcinogenesis. However, these mitochondrial processes remain to be investigated in OC. Eighteen controls and 16 OC tissues (serous and mucinous) were collected. Enzymatic activities were performed spectrophotometrically,
mitochondrial DNA (
mtDNA) content was measured by real-time-PCR,
protein levels were determined by Western blotting, and mitochondrial number and structure were measured by electron microscopy. Statistical analysis was performed using Student's t-test, Mann-Whitney U test, and principal component analysis (PCA). We found, in OC, that increased mitochondrial number associated with increased
peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) and
mitochondrial transcription factor A (TFAM)
protein levels, as well as
mtDNA content. The OC mitochondria presented an increased maximum length, as well as reduced cristae width and junction diameter, associated with increased
optic atrophy 1 protein (OPA1) and
prohibitin 2 (PHB2)
protein levels. In addition, in OC tissues, augmented cAMP and
sirtuin 3 (
SIRT3)
protein levels were observed. PCA of the 25 analyzed biochemical parameters classified OC patients in a distinct group from controls. We highlight a "mitochondrial signature" in OC that could result from cooperation of the cAMP pathway with the
SIRT3, OPA1, and PHB2
proteins.