OPA1 and breast cancer: However, while genetic or pharmacological OPA1 inhibition induced the expected mitochondrial fragmentation in MDA-MB231 cells (Fig. 5a-g), mitochondrial membrane potential, ATP level and mitochondrial respiration were not affected in OPA1-silenced and OPA1-ablated MDA-MB-231 (Fig. 5 h-j). Another potential explanation for the pleiotropic effects observed upon OPA1 deletion in breast cancer cells was the potential regulation of miRNAs that can control multiple cellular pathways by seeding on a variety of different 3’UTRs.