In previous studies, we showed that MIRO2 mRNA is up-regulated in primary cancer versus normal tissues, across multiple tumor types. MIRO2 had been previously studied in the context of non-tumorigenic cells, where it coordinates microtubule- and actin-based mitochondrial movement. However, we showed that cancer cells utilize MIRO2’s canonical function on mitochondrial trafficking exclusively under conditions of cellular stress that exacerbate mitochondrial dynamics. Thus, identifying MIRO2’s protein binding partners would shed light on the molecular function of MIRO2 in prostate cancer. To this end, we identified the proteins co-precipitating with FLAG-MIRO2 from PC3 cells. Network analysis of MIRO2 binding partners identified metabolism, cell cycle and cellular responses to extracellular stimuli amongst the top over-represented pathways.