Redox Regulation of Cancer Metastasis: Molecular Signaling and Therapeutic Opportunities

被引:34
作者
Yang, Wenyong [1 ,2 ,3 ,4 ]
Zou, Linzhi [1 ,2 ,3 ,4 ]
Huang, Canhua [4 ]
Lei, Yunlong [1 ,2 ]
机构
[1] Chongqing Med Univ, Dept Biochem & Mol Biol, Chongqing 400016, Peoples R China
[2] Chongqing Med Univ, Mol Med & Canc Res Ctr, Chongqing 400016, Peoples R China
[3] Sichuan Univ, Coll Life Sci, Chengdu 610065, Peoples R China
[4] Sichuan Univ, West China Hosp, State Key Lab Biotherapy, Chengdu 610041, Peoples R China
关键词
cancer therapy; metastasis; reactive oxygen species; redox sensors; NF-KAPPA-B; MITOCHONDRIAL PERMEABILITY TRANSITION; ENDOTHELIAL GROWTH-FACTOR; SRC TYROSINE KINASE; OXIDATIVE STRESS; PROTEASOME INHIBITOR; S-GLUTATHIONYLATION; ANOIKIS RESISTANCE; TUMOR PROGRESSION; GENE-EXPRESSION;
D O I
10.1002/ddr.21216
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Cancer metastasis is the major cause of cancer-related mortality. Accumulated evidence has shown that high-metastasis potential cancer cells have more reactive oxygen species (ROS) accumulation compared with low-metastasis potential cancer cells. ROS can function as second messengers to regulate multiple cancer metastasis-related signaling pathways via reversible oxidative posttranslational modifications of cysteine in key redox-sensitive proteins, which leads to the structural and functional change of these proteins. Because ROS can promote cancer metastasis, therapeutic strategies aiming at inducing/reducing cellular ROS level or targeting redox sensors involved in metastasis hold great potential in developing new efficient approaches for anticancer therapy. In this review, we summarize recent findings on regulation of tumor metastasis by key redox sensors and describe the potential of targeting redox signaling pathways for cancer therapy. (C) 2014 Wiley Periodicals, Inc.
引用
收藏
页码:331 / 341
页数:11
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