Caveolin-1 is involved in DNA damage and repair signaling in X-irradiated Chang liver cells.
- Author:
Hong-Yan LI
1
;
Chao QU
1
;
Ye-Jun ZHANG
1
;
Jia SUN
1
;
Chao HAN
2
;
Jing LIU
3
;
Wei ZOU
4
Author Information
1. College of Life Science, Liaoning Normal University, Dalian 116081, China.
2. Regenerative Medicine Centre, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, China.
3. Regenerative Medicine Centre, the First Affiliated Hospital of Dalian Medical University, Dalian 116011, China. liujing.dlrmc@hotmail.com.
4. College of Life Science, Liaoning Normal University, Dalian 116081, China. weizou60@126.com.
- Publication Type:Journal Article
- From:
Acta Physiologica Sinica
2017;69(6):759-766
- CountryChina
- Language:English
-
Abstract:
Caveolin-1 (Cav-1), as an important structural protein of caveolae, has been proven to be correlated with several signal transduction pathways. Recent studies have shown that Cav-1 may play a critical role in response to DNA damage in irradiated pancreatic cancer cells. However, it is not known whether down-regulation of Cav-1 is required to enhance the damage of other kinds of human cells exposed to X-radiation. In this study, the role of Cav-1 in Chang liver cell line (CHL) exposed to X-radiation was investigated. Cav-1 knockdown cell line (CHL-CAV7) was stably established by the siRNA plasmids transfection, and Cav-1 expression was suppressed by 60%, compared with that of control group (CHL-C) which was transfected with non-targeting plasmids. Cellular survival ability and the expressions of proteins related to DNA damage and repair were examined by colony formation assay and Western blot, respectively. Down-regulation of Cav-1 expression induced a significant decrease of the survival rate in CHL-CAV7 cells exposed to 8 and 10 Gy X-radiation. Compared with CHL-C cells, CHL-CAV7 cells showed increased γH2AX expression, as well as decreased p-ATM, DNA-dependent protein kinase, catalytic subunit (DNA-PKcs) and p53 protein expressions when treated with X-radiation. Meanwhile, the colocalization of Mdm2 and Cav-1 was decreased in CHL-CAV7 cells compared with that in CHL-C cells. These results suggest that the down-regulation of Cav-1 may aggravate DNA damage of CHL cells through reducing the interaction of Cav-1 and Mdm2, which results in the promotion of p53 degradation.
