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ER stress‐induced autophagy in melanoma
Author(s) -
Meng XiaoXiao,
Yao Mu,
Zhang Xu Dong,
Xu HongXi,
Dong Qihan
Publication year - 2015
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12436
Subject(s) - autophagy , melanoma , unfolded protein response , cancer research , mapk/erk pathway , endoplasmic reticulum , biology , kinase , microbiology and biotechnology , v600e , mutation , apoptosis , biochemistry , gene
Summary The activation of RAF ‐ MEK –extracellular signal‐regulated kinase ( ERK ) mitogen‐activated protein kinase cascade by v‐raf murine sarcoma viral oncogene homolog B1 ( BRAF ) V600E mutation is a key alteration in melanoma. Although BRAF inhibitor ( BRAF i) has achieved remarkable clinical success, the positive response to BRAF i is not sustainable, and the initial clinical benefit is eventually barred by the development of resistance to BRAF i. There is growing evidence to suggest that endoplasmic reticulum ( ER ) stress‐induced autophagy could be a potential pro‐survival mechanism that contributes to genesis of melanoma and to the resistance to BRAF i. ER stress‐induced autophagy is an evolutionarily conserved membrane process. By degrading and recycling proteins and organelles via the formation of autophagous vesicles and their fusion with lysosomes, the autophagy plays a key role in homeostasis as well as pathological processes. In this review, we examine the autophagy phenomenon in melanocytic nevus, primary and metastatic melanoma, and its significance in BRAF i‐resistant melanoma.