Li Yanping, Liang Ronghui, Zhang Xiaoya, Wang Jiyan, Shan Changliang, Liu Shuangping, Li Leilei, Zhang Shuai
Biomedical Translational Research Institute, Jinan University, Guangzhou, China.
State Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin, China.
Front Pharmacol. 2019 Apr 5;10:356. doi: 10.3389/fphar.2019.00356. eCollection 2019.
Copper chaperone for superoxide dismutase (CCS) is a critical component of oxidation-reduction system and functions as a potential tumor promoter in several cancers. However, the function and clinical significance of CCS in breast cancer remain unclear. Here, we found CCS was highly expressed in breast cancer, where it promoted breast cancer cell proliferation and migration. Suppression of CCS expression was sufficient to attenuate the phosphorylation level of ERK1/2 and increase the accumulation of reactive oxygen species (ROS). Mechanistically, we found that knockdown of CCS decreases the activity of ERK1/2 mediated by the accumulation of ROS, which leads to the inhibition of cell proliferation and migration. In summary, these results indicated that CCS promotes the growth and migration of breast cancer cells regulating the ERK1/2 activity mediated by ROS.
超氧化物歧化酶铜伴侣蛋白（CCS）是氧化还原系统的关键组成部分，在多种癌症中作为潜在的肿瘤促进因子发挥作用。然而，CCS在乳腺癌中的功能和临床意义仍不清楚。在此，我们发现CCS在乳腺癌中高表达，它促进乳腺癌细胞的增殖和迁移。抑制CCS表达足以降低ERK1/2的磷酸化水平并增加活性氧（ROS）的积累。机制上，我们发现敲低CCS会降低由ROS积累介导的ERK1/2活性，从而导致细胞增殖和迁移受到抑制。总之，这些结果表明CCS通过调节由ROS介导的ERK1/2活性促进乳腺癌细胞的生长和迁移。
