Abstract
Mitochondria, as the main site of cellular energy metabolism and the generation of oxygen free radicals, are the key switch for mitochondria-mediated endogenous apoptosis. Ca(2+) is not only an important messenger for cell proliferation, but it is also an indispensable signal for cell death. Ca(2+) participates in and plays a crucial role in the energy metabolism, physiology, and pathology of mitochondria. Mitochondria control the uptake and release of Ca(2+) through channels/transporters, such as the mitochondrial calcium uniporter (MCU), and influence the concentration of Ca(2+) in both mitochondria and cytoplasm, thereby regulating cellular Ca(2+) homeostasis. Mitochondrial Ca(2+) transport-related processes are involved in important biological processes of tumor cells including proliferation, metabolism, and apoptosis. In particular, MCU and its regulatory proteins represent a new era in the study of MCU-mediated mitochondrial Ca(2+) homeostasis in tumors. Through an in-depth analysis of the close correlation between mitochondrial Ca(2+) and energy metabolism, autophagy, and apoptosis of tumor cells, we can provide a valuable reference for further understanding of how mitochondrial Ca(2+) regulation helps diagnosis and therapy.