Zhai Lu1, Hua Chen2, Xiao-Mei Zheng1, Man-Ling Chen1. 1. Affiliated Hospital of Hainan Medical University, Haikou 570102, China. 2. Affiliated Hospital of Hainan Medical University, Haikou 570102, China. Electronic address: 15808943486@163.com.
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.
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.