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Biochim Biophys Acta Mol Cell Res. 2017 Jun;1864(6):858-864. doi: 10.1016/j.bbamcr.2016.12.024. Epub 2017 Jan 4.

Endoplasmic reticulum-mitochondria Ca2+ crosstalk in the control of the tumor cell fate.

Author information

1
Dept. of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy.
2
KWS BioTest, Marine View Office Park, Portishead, Somerset BS20 7AW, UK.
3
Department of Morphology, Surgery and Experimental Medicine, Section of Human Anatomy and Histology, Laboratory for Technologies of Advanced Therapies(LTTA), University of Ferrara, Ferrara, Italy.
4
Dept. of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy. Electronic address: paolo.pinton@unife.it.

Abstract

Mitochondria-associated membranes are juxtaposed between the endoplasmic reticulum and mitochondria and have been identified as a critical hub in the regulation of apoptosis and tumor growth. One key function of mitochondria-associated membranes is to provide asylum to a number of proteins with tumor suppressor and oncogenic properties. In this review, we discuss how Ca2+ flux manipulation represents the primary mechanism underlying the action of several oncogenes and tumor-suppressor genes and how these networks might be manipulated to provide novel therapies for cancer. This article is part of a Special Issue entitled: ECS Meeting edited by Claus Heizmann, Joachim Krebs and Jacques Haiech.

PMID:
28064002
DOI:
10.1016/j.bbamcr.2016.12.024
[Indexed for MEDLINE]
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