Realgar-lnduced Apoptosis of Cervical Cancer Cell Line Siha via Cytochrome C Release and Caspase-3 and Caspase-9 Activation

Objective: To explore the molecular mechanism of realgar-induced apoptosis of cervical cancer cells. Methods: The cervical cancer cell line Siha was used to determine the cell viability and apoptosis after treatment with realgar using MTT assay and flow cytometry. The activities of caspase-3, -8, an...

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Published in:中国结合医学杂志:英文版 Vol. 18; no. 5; pp. 359 - 365
Main Author: 程艳香 刘嵘 王琴 李秉枢 许学先 胡敏 陈璐 付琼 濮德敏 洪莉
Format: Journal Article
Language:English
Published: 2012
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Summary:Objective: To explore the molecular mechanism of realgar-induced apoptosis of cervical cancer cells. Methods: The cervical cancer cell line Siha was used to determine the cell viability and apoptosis after treatment with realgar using MTT assay and flow cytometry. The activities of caspase-3, -8, and -9 were detected by fluorescence resonance energy transfer technology and colorimetric assay, while the levels of Bcl-2, cytochrome c, and Bax were detected by Western blot method. Results: Induction of apoptosis by realgar was detected in Siha cell line in a dose-dependent manner. The apoptosis was accompanied by a significant increase in cytochrome c release and activation of caspase-3 and caspase-9 but not caspase-8. Further, the realgar-induced apoptosis was inhibited by a broad-spectrum caspase inhibitor, a caspase-3 inhibitor, and a caspase-9 inhibitor but not by a caspase-8 inhibitor. Bcl-2 and Bax protein expressions were not changed by realgar. Conclusion: The induction of apoptosis by realgar is mediated through a cytochrome c-dependent pathway, which sequentially activates caspase-9 and caspase-3.
Bibliography:realgar, cervical cancer, apoptosis, cytochrome c, caspases
11-4928/R
Objective: To explore the molecular mechanism of realgar-induced apoptosis of cervical cancer cells. Methods: The cervical cancer cell line Siha was used to determine the cell viability and apoptosis after treatment with realgar using MTT assay and flow cytometry. The activities of caspase-3, -8, and -9 were detected by fluorescence resonance energy transfer technology and colorimetric assay, while the levels of Bcl-2, cytochrome c, and Bax were detected by Western blot method. Results: Induction of apoptosis by realgar was detected in Siha cell line in a dose-dependent manner. The apoptosis was accompanied by a significant increase in cytochrome c release and activation of caspase-3 and caspase-9 but not caspase-8. Further, the realgar-induced apoptosis was inhibited by a broad-spectrum caspase inhibitor, a caspase-3 inhibitor, and a caspase-9 inhibitor but not by a caspase-8 inhibitor. Bcl-2 and Bax protein expressions were not changed by realgar. Conclusion: The induction of apoptosis by realgar is mediated through a cytochrome c-dependent pathway, which sequentially activates caspase-9 and caspase-3.
ISSN:1672-0415
1993-0402