New Insights into the Role of Endoplasmic Reticulum Stress in Breast Cancer Metastasis

被引:7
|
作者
Han, Chang-chang [1 ,2 ]
Wan, Fu-sheng [1 ]
机构
[1] Nanchang Univ, Sch Basic Med, Dept Biochem & Mol Biol, 461 Bayi Ave, Nanchang 330006, Jiangxi, Peoples R China
[2] Suqian First Hosp, Ctr Prenatal Diag, Suqian, Peoples R China
基金
中国国家自然科学基金;
关键词
Breast neoplasms; Endoplasmic reticulum stress; Neoplasm metastasis; Unfolded protein response; GLUCOSE-REGULATED PROTEINS; TO-MESENCHYMAL TRANSITION; TYROSINE-PHOSPHATASE; 1B; MITOCHONDRIAL APOPTOTIC PATHWAY; ER STRESS; IN-VITRO; TUMOR-SUPPRESSOR; GRP78; PROMOTES; CELL-SURVIVAL; AUTOPHAGY;
D O I
10.4048/jbc.2018.21.e51
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cellular stress severely disrupts endoplasmic reticulum (ER) function, leading to the abnormal accumulation of unfolded or misfolded proteins in the ER and subsequent development of endoplasmic reticulum stress (ERS). To accommodate the occurrence of ERS, cells have evolved a highly conserved, self-protecting signal transduction pathway called the unfolded protein response. Notably, ERS signaling is involved in the development of a variety of diseases and is closely related to tumor development, particularly in breast cancer. This review discusses recent research regarding associations between ERS and tumor metastasis. The information presented here will help researchers elucidate the precise mechanisms underlying ERS-mediated tumor metastasis and provide new directions for tumor therapies.
引用
收藏
页码:354 / 362
页数:9
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