title: Mitochondrial calcium uniporter, MiRNA and cancer: Live and let die.
abstract: Mitochondria receive calcium (Ca(2+)) signals from endoplasmic reticulum (ER) and decode them into pro-apoptotic inputs, which lead to cell death. Therefore, mitochondrial Ca(2+) overload is considered a fundamental trigger of the apoptotic process, and several oncogenes and tumor suppressors modify the activity of protein involved in Ca(2+) homeostasis to control apoptosis. The identification of the channel responsible for mitochondrial Ca(2+) entry, the Mitochondrial Ca(2+)Uniporter (MCU), together with its regulatory components, MICU1 and MCUR1, provides new molecular tools to investigate this process. Recent data have also shown that miR-25 decreases mitochondrial Ca(2+) uptake through selective MCU downregulation, conferring resistance to apoptotic challenges. MCU appears to be downregulated in human colon cancer samples, and accordingly, miR-25 is aberrantly expressed, indicating the importance of mitochondrial Ca(2+) regulation in cancer cell survival.
authors.affiliation: Department of Morphology; Surgery and Experimental Medicine; Section of General Pathology; Interdisciplinary Center for the Study of Inflammation (ICSI); Laboratory for Technologies of Advanced Therapies (LTTA); University of Ferrara; Ferrara, Italy.
authors.forename: Saverio
authors.initials: S
authors.lastname: Marchi
authors.forename: Paolo
authors.initials: P
authors.lastname: Pinton
keywords: MicroRNAs (MiRNA); Mitochondrial Calcium Uniporter (MCU); apoptosis; calcium (Ca2+); cancer; cell death; mitochondria