[an error occurred while processing this directive]

Hereditas(Beijing) ›› 2019, Vol. 41 ›› Issue (4): 318-326.doi: 10.16288/j.yczz.18-278

• Research Article • Previous Articles     Next Articles

Effects of CSN4 knockdown on proliferation and apoptosis of breast cancer MDA-MB-231 cells

Tonglu YU1,2,Dongliang Cai1,2,Genfeng Zhu1,2,Xiaojuan Ye1,2,Taishan Min1,2,Hongyan Chen1,2,Daru Lu1,2,Haoming Chen1,2()   

  1. 1. School of Life Sciences, Fudan University, Shanghai 200438, China
    2. MOE Key Laboratory of Contemporary Anthropology, Fudan University, Shanghai 200438, China
  • Received:2018-12-11 Revised:2019-02-18 Online:2019-04-20 Published:2019-03-15
  • Contact: Chen Haoming E-mail:hmchen@fudan.edu.cn
  • Supported by:
    the National Natural Science Foundation of China(81071739);the National Natural Science Foundation of China(81272385)

Abstract:

Breast cancer is one of the most common malignant tumors endangering women. It has been found that the subunits of the COP9 complex are closely related to the occurrence and development of malignant tumors, and the CSN4 subunit plays an important role in regulating the whole complex. In the breast cancer cell line MDA-MB-231, we successfully established a lentivirus-mediated CSN4-knockdown cell line. CCK8 cell proliferation assays and colony formation experiments confirmed that CSN4 knockdown significantly decreased the cellular proliferation rate. Cell cycle analysis showed that CSN4 knockdown increased sub-G1 population and induced apoptosis. In addition, Western blotting assays confirmed that CSN4 regulates the expression of CDK6 and Caspase3, suggesting that CSN4 modulates the proliferation and apoptosis of breast cancer cells by regulating the expression of CDK6 and Caspase3 genes and thereby tumorigenesis. This study has deepened our understanding of the molecular mechanism of apoptosis and cell growth in breast cancers, and further revealed the role and mechanism of CSN4 in cancer biology.

Key words: breast cancer, CSN4, cell proliferation, cell apoptosis, CDK6, Caspase3