Mitochondria-Associated endoplasmic reticulum Membranes (MAMs) microenvironment: targeting autophagic and apoptotic pathways in cancer therapy

Frontiers in Oncology. 2015;5 DOI 10.3389/fonc.2015.00173

 

Journal Homepage

Journal Title: Frontiers in Oncology

ISSN: 2234-943X (Online)

Publisher: Frontiers Media S.A.

LCC Subject Category: Medicine: Internal medicine: Neoplasms. Tumors. Oncology. Including cancer and carcinogens

Country of publisher: Switzerland

Language of fulltext: English

Full-text formats available: PDF, HTML, ePUB, XML

 

AUTHORS

Simone ePatergnani (University of Ferrara)
Sonia eMissiroli (University of Ferrara)
Saverio eMarchi (University of Ferrara)
Carlotta eGiorgi (University of Ferrara)

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 14 weeks

 

Abstract | Full Text

Autophagy is a tightly regulated catabolic pathway that terminates in the lysosomal compartment after the formation of a cytoplasmic vacuole that engulfs macromolecules and organelles. Notably, autophagy is associated with several human pathophysiological conditions, playing either a cytoprotective or cytopathic role. Many studies have investigated the role of autophagy in cancer. However, whether autophagy suppresses tumorigenesis or provides cancer cells with a rescue mechanism under unfavorable conditions remains unclear. Mitochondria-associated membranes (MAMs) 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 MAMs is to provide asylum to a number of proteins with tumor suppressor and oncogenic properties. Accordingly, mechanistic studies during tumor progression suggest a strong involvement of these proteins at various steps of the autophagic process. This paper discusses the present state of our knowledge about the intimate molecular networks between MAMs and autophagy in cancer cells and addresses how these networks might be manipulated to improve anticancer therapeutics.