Journal
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
Volume 1858, Issue 8, Pages 615-627Publisher
ELSEVIER
DOI: 10.1016/j.bbabio.2017.01.003
Keywords
Calcium (Ca2+); Apoptosis; Autophagy; Mitochondria associated membranes (MAMs); Endoplasmic reticulum; Tumor
Categories
Funding
- Telethon [GGP15219/B]
- Italian Association for Cancer Research (AIRC) [IG-18624]
- Italian Cystic Fibrosis Research Foundation
- Italian Ministry of Education, University and Research (COFIN) [20129JIASY_002]
- Italian Ministry of Education, University and Research (FIRB) [RBAP11FXBC_002]
- Futuro in Ricerca [RBFR10EGVP_001]
- University of Ferrara
- Italian Ministry of Health
- AIRC [MFAG-13521]
- Italian Ministry of Health, Cariplo
- FISM Fondazione Italiana Sclerosi Multipla [2014/B/3]
- Polish National Science Centre [UM0-2014/15/B/NZ1/00490]
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Until 1972, the term 'apoptosis' was used to differentiate the programmed cell death that naturally occurs in organismal development from the acute tissue death referred to as necrosis. Many studies on cell death and programmed cell death have been published and most are, at least to some degree, related to cancer. Some key proteins and molecular pathways implicated in cell death have been analyzed, whereas others are still being actively researched; therefore, an increasing number of cellular compartments and organelles are being implicated in cell death and cancer. Here, we discuss the mitochondria and subdomains of the endoplasmic reticulum (ER) that interact with mitochondria, the mitochondria-associated membranes (MAMs), which have been identified as critical hubs in the regulation of cell death and tumor growth. MAMs-dependent calcium (Ca2+) release from the ER allows selective Ca2+ uptake by the mitochondria. The perturbation of Ca2+ homeostasis in cancer cells is correlated with sustained cell proliferation and the inhibition of cell death through the modulation of Ca2+ signaling. This article is part of a Special Issue entitled Mitochondria in Cancer, edited by Giuseppe Gasparre, Rodrigue Rossignol and Pierre Sonveaux. (C) 2017 Elsevier B.V. All rights reserved.
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