Metabolic disorders and cancer: Store-operated Ca2+ entry in cancer: Focus on IP3R-mediated Ca2+ release from intracellular stores and its role in migration and invasion

Abstract

Store-operated calcium entry (SOCE) plays important roles in a multitude of cellular processes, from muscle contraction to cellular proliferation and migration. Dysregulation of SOCE is responsible for the advancement of multiple diseases, ranging from immune diseases, myopathies, to terminal ones like cancer. Naturally, SOCE has been a focus of many studies and review papers which, however, primarily concentrated on the principal players localized to the plasma membrane and responsible for Ca2+ entry into the cell. Much less has been said about other players participating in the entire SOCE event. This review aims to address this shortcoming by discussing the accumulated scientific knowledge focused on the inositol trisphosphate receptors (IP3Rs), principal player responsible for emptying intracellular Ca2+ stores in a majority of cells, and their involvement in regulation of cell migration and invasion in cancer.