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: Saverio Marchi, Paolo Pinton
• Journal: Communicative & integrative biology (Commun Integr Biol) Vol. 6 Issue 3 Pg. e23818 (May 01 2013) ISSN: 1942-0889 [Print] United States
• PMID: 23713134 (Publication Type: Journal Article)