Author:

Keywords:

Science & Technology, Life Sciences & Biomedicine, Cell Biology, Medicine, Research & Experimental, Research & Experimental Medicine, Calcium signaling, Ca2+ -transport systems, IP3 receptors, Voltage-dependent anion channels, Chaperones, Cell death and survival, Mitochondrial bioenergetics, Autophagy, Mitochondria-associated ER membranes (MAMs), Cancer, DEPENDENT ANION CHANNEL, INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR, ENDOPLASMIC-RETICULUM STRESS, UNFOLDED PROTEIN RESPONSE, PERMEABILITY TRANSITION PORE, WILD-TYPE P53, SIGMA-1 RECEPTOR, BH4 DOMAIN, CELL-SURVIVAL, INDUCED APOPTOSIS, Ca2+-transport systems, Animals, Calcium Signaling, Endoplasmic Reticulum, Humans, Intracellular Membranes, Membrane Microdomains, Membrane Proteins, Mitochondria, Mitochondrial Proteins, Neoplasms, Tumor Microenvironment, 11 Medical and Health Sciences, General & Internal Medicine, 31 Biological sciences, 32 Biomedical and clinical sciences

Abstract:

Inter-organellar contact sites establish microdomains for localised Ca2+-signalling events. One of these microdomains is established between the ER and the mitochondria. Importantly, the so-called mitochondria-associated ER membranes (MAMs) contain, besides structural proteins and proteins involved in lipid exchange, several Ca2+-transport systems, mediating efficient Ca2+ transfer from the ER to the mitochondria. These Ca2+ signals critically control several mitochondrial functions, thereby impacting cell metabolism, cell death and survival, proliferation and migration. Hence, the MAMs have emerged as critical signalling hubs in physiology, while their dysregulation is an important factor that drives or at least contributes to oncogenesis and tumour progression. In this book chapter, we will provide an overview of the role of the MAMs in cell function and how alterations in the MAM composition contribute to oncogenic features and behaviours.