Cell fate is critically affected by mitochondrial activity, from ATP production to metabolism, Ca2+ homeostasis and signaling. These actions are regulated by proteins expressed in mitochondria (Mt)‑endoplasmic reticulum contact sites (MERCSs). The literature supports the fact that disruption to the physiology of the Mt and/or MERCSs can be due to alterations in the Ca2+ influx/efflux, which further regulates autophagy and apoptosis activity. The current review presents the findings of numerous studies with regard to the involvement of proteins positioned in MERCSs and how they express anti‑ and pro‑apoptotic properties by adjusting Ca2+ across membranes. The review also explores the involvement of mitochondrial proteins as hot spots in cancer development, cell death and/or survival, and the method via which they can potentially be targeted as a therapeutic option.
Keywords: Ca2+ singling; MERCS; MERCS genes; cancer.