The ER-mitochondria Ca 2+ signaling in cancer progression: Fueling the monster.

Autor:	Bustos G; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile., Ahumada-Castro U; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile., Silva-Pavez E; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile., Puebla A; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile., Lovy A; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile; Department of Neuroscience, Center for Neuroscience Research, Tufts School of Medicine, Boston, MA, United States. Electronic address: alenka.lovy@umayor.cl., Cesar Cardenas J; Faculty of Sciences, Universidad Mayor, Center for Integrative Biology, Santiago, Chile; Geroscience Center for Brain Health and Metabolism, Santiago, Chile; Buck Institute for Research on Aging, Novato, CA, United States; Department of Chemistry and Biochemistry, University of California, Santa Barbara, CA, United States. Electronic address: julio.cardenas@umayor.cl.
Jazyk:	angličtina
Zdroj:	International review of cell and molecular biology [Int Rev Cell Mol Biol] 2021; Vol. 363, pp. 49-121. Date of Electronic Publication: 2021 Apr 12.
DOI:	10.1016/bs.ircmb.2021.03.006
Abstrakt:	Cancer is a leading cause of death worldwide. All major tumor suppressors and oncogenes are now recognized to have fundamental connections with metabolic pathways. A hallmark feature of cancer cells is a reprogramming of their metabolism even when nutrients are available. Increasing evidence indicates that most cancer cells rely on mitochondrial metabolism to sustain their energetic and biosynthetic demands. Mitochondria are functionally and physically coupled to the endoplasmic reticulum (ER), the major calcium (Ca 2+ ) storage organelle in mammalian cells, through special domains known as mitochondria-ER contact sites (MERCS). In this domain, the release of Ca 2+ from the ER is mainly regulated by inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs), a family of Ca 2+ release channels activated by the ligand IP3. IP3R mediated Ca 2+ release is transferred to mitochondria through the mitochondrial Ca 2+ uniporter (MCU). Once in the mitochondrial matrix, Ca 2+ activates several proteins that stimulate mitochondrial performance. The role of IP3R and MCU in cancer, as well as the other proteins that enable the Ca 2+ communication between these two organelles is just beginning to be understood. Here, we describe the function of the main players of the ER mitochondrial Ca 2+ communication and discuss how this particular signal may contribute to the rise and development of cancer traits. (Copyright © 2021 Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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