期刊
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
卷 27, 期 7, 页码 906-919出版社
WILEY
DOI: 10.1111/jcmm.17696
关键词
autophagy; calcium transfer; cancer; endoplasmic reticulum; ER stress; lipid synthesis; mitochondria; mitochondrial-associated membrane
The mitochondrial-associated membrane (MAM) is a platform that promotes communication between the endoplasmic reticulum (ER) and mitochondria. It plays a crucial role in various physiological processes and its dysregulation can impact cancer cell fate. This review summarizes the structure of MAM and the functions of MAM-resident proteins in tumorigenesis, and discusses the mechanisms by which natural compounds induce cancer cell apoptosis through ER stress.
The mitochondrial-associated membrane (MAM) is a physical platform that facilitates communication between the endoplasmic reticulum (ER) and mitochondria. It is enriched with many proteins and enzymes and plays an important role in the regulation of several fundamental physiological processes, such as calcium (Ca2+) transfer, lipid synthesis, cellular autophagy and ER stress. Accumulating evidence suggests that oncogenes and suppressor genes are present at the ER-mitochondrial contact site, and their alterations can affect Ca2+ flux, lipid homeostasis, and the dysregulation of mitochondrial dynamics, thereby influencing the fate of cancer cells. Understanding the fundamental role of MAM-resident proteins in tumorigenesis could support the search for novel therapeutic targets in cancer. In this review, we summarize the basic structure of MAM and the core functions of MAM-resident proteins in tumorigenesis. In addition, we discuss the mechanisms by which natural compounds promote cancer cell apoptosis from the perspective of ER stress.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据