Mitochondrial membrane potential regulation is independent of c-fos expression

Tumour cells contain mitochondria with elevated membrane potentials compare d with normal cells, and thus this feature provides a selective target for destroying tumour cells. To improve mitochondrial-based therapies, a better understanding of the factors involved in regulating mitochondria are requi red. Since v-fos overexpression has been shown to elevate mitochondrial mem brane potentials in rat fibroblasts, we investigated whether the human homo logue, c-fos, was also capable of regulating the mitochondrial membrane pot ential in cells. Rat fibroblasts transfected with the c-fos gene did not ac cumulate more rhodamine 123 (Rh123) nor did they retain this Rh123 for exte nded periods of time compared with their parental line. Moreover, there was no difference in survival following dequalinium chloride (Deca) treatment between transfectants and controls. Similarly, reduction of c-fos expressio n in rat fibroblasts did not significantly alter their mitochondrial membra ne potential. In addition, human ovarian carcinoma cells, which overexpress the c-fos gene, did not accumulate more Rh123 nor were they hypersensitive to Deca compared with their parental line. In another human ovarian carcin oma cell Line, selection of variants with lower mitochondrial membrane pote ntial did not alter c-fos mRNA or protein levels. These data suggest that a lterations in c-fos expression do not regulate the magnitude of the mitocho ndrial membrane potential.