Abstract
Mitochondria-associated ER membranes (MAMs) represent a crucial intracellular signaling hub, that regulates various cellular events including Ca2+ homeostasis, lipid metabolism, mitochondrial function, and cellular survival and death. All of these MAM-mediated cellular events contribute to carcinogenesis. Indeed, altered functions of MAMs in several types of cancers have been documented, in particular for breast cancer. Over the past years, altered expression of many MAM-resident proteins have been reported in breast cancer. These MAM-resident proteins play an important role in regulation of breast cancer initiation and progression. In the current review, we discuss our current knowledge about the functions of MAMs, and address the underlying mechanisms through which MAM-resident proteins regulate breast cancer. A fuller understanding of the pathways through which MAMs regulate breast cancer, and identification of breast cancer-specific MAM-resident proteins may help to develop novel therapeutic strategies for breast cancer.
Highlights
The interconnection between mitochondria and endoplasmic reticulum was the first inter-organelle contact site discovered in the late 1950’s (Bernhard and Rouiller, 1956)
Over the past few decades, extensive researches have reported that mitochondria-associated endoplasmic reticulum membranes (MAMs) act as signaling hubs that control endoplasmic reticulum (ER) and mitochondrial biology, and disturbances of MAMs result in dysfunctions in a wide range of cellular processes including apoptosis, inflammation, and autophagy (Morciano et al, 2018)
Cell-death-pathway-involved proteins in MAMs such as BCL2, p53 tumor suppressor, NLRP3 and their related proteins have been widely investigated for prognosis and targeted anti-cancer therapy
Summary
The interconnection between mitochondria and endoplasmic reticulum was the first inter-organelle contact site discovered in the late 1950’s (Bernhard and Rouiller, 1956). Several subsequent fractionation studies have successfully isolated mitochondria-associated endoplasmic reticulum membranes (MAMs) as a distinct and purified structure from liver cells (Wanson et al, 1975; Pickett et al, 1981; Katz et al, 1983). Over the past few decades, extensive researches have reported that MAMs act as signaling hubs that control ER and mitochondrial biology, and disturbances of MAMs result in dysfunctions in a wide range of cellular processes including apoptosis, inflammation, and autophagy (Morciano et al, 2018). These cellular activities have crucial roles in several pathologies including but not limited to cardiovascular disease and cancer. We will highlight the multiple physiological functions of MAMs in mitochondrial Ca2+ signaling, metabolism and autophagy, and discuss how alterations in MAMs contribute to carcinogenesis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
