Experimental study on the apoptosis of cervical cancer Hela cells induced by juglone through c-Jun N-terminal kinase/c-Jun pathway
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 SP6...
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Veröffentlicht in: | Asian Pacific journal of tropical medicine 2017-06, Vol.10 (6), p.641-644 |
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Sprache: | eng |
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Zusammenfassung: | 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, Cyt C, Fas, Fas L, 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, Cyt C, Fas, Fas L, 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, Cyt C, Fas, Fas L 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, Cyt C, Fas, Fas L 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. |
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ISSN: | 1995-7645 2352-4146 |
DOI: | 10.1016/j.apjtm.2017.06.005 |