Experimental study on the apoptosis of cervical cancer Hela cells induced by juglone through c-Jun N-terminal kinase/c-Jun pathway
10.1016/j.apjtm.2017.06.005
- Author:
Zhai LU
1
;
Hua CHEN
1
;
Xiao-Mei ZHENG
1
;
Man-Ling CHEN
1
Author Information
1. Affiliated Hospital of Hainan Medical University
- Publication Type:Journal Article
- Keywords:
Apoptosis;
c-Jun N-terminal kinase;
Cervical cancer;
Death receptor;
Juglone;
Mitochondria
- From:
Asian Pacific Journal of Tropical Medicine
2017;10(6):572-575
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the regulatory effect and molecular mechanism of juglone on apoptosis of cervical cancer Hela cells. Methods Cervical cancer Hela cells were cultured and treated with different dosages of juglone (10, 20, and 40 μmol/L, respectively) and c-Jun N-terminal kinase (JNK) inhibitor SP600125 (10, 20, and 40 μmol/L, respectively). Then cellular proliferative activity and the expression of JNK/c-Jun pathway molecule and apoptotic molecule in the cells were detected. Results After 6, 12, 18 and 24 h of treatment, the value for proliferative activity of cells treated with juglone was significantly lower than that of control group (P < 0.05), and the anti-proliferative effect was more significant as the treatment period and juglone dosage increased (P < 0.05). The protein expressions of Bax, CytC, Fas, FasL, Caspase-3, p-JNK and p-c-Jun in cells treated with juglone were significantly higher than those of control group (P < 0.05), and the protein expressions of Bax, CytC, Fas, FasL, Caspase-3, p-JNK and p-c-Jun increased more remarkably as the juglone dosage increased (P < 0.05). In cells treated with 40 μmol/L juglone and SP600125, the protein expressions of Bax, CytC, Fas, FasL and Caspase-3 were significantly lower than those of cells treated with 40 μmol/L juglone (P < 0.05), and the protein expressions of Bax, CytC, Fas, FasL and Caspase-3 reduced more remarkably as the SP600125 dosage increased (P < 0.05). Conclusion Juglone can increase the expression of apoptotic molecules in mitochondrial pathway and death receptor pathway by activating JNK/c-Jun pathway, thus inducing apoptosis of cervical cancer cells.
