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Published on: December 21, 2019
β-elemene induces glioma cell apoptosis by downregulating survivin and its interaction with hepatitis B
Hang Zhang1, Feng Xu, Tian Xie
1Department of Basic Medical Science, Hangzhou Normal University, Hangzhou, Zhejiang, PR China.
Abstract:
β-elemene, extracted from the ginger plant, possesses antitumor activity against a broad range of cancers clinically. However, the mechanism underlying β-elemene-induced cytotoxicity remains incompletely understood. Here, we show that β-elemene promoted apoptotic cell death in human glioma cells, downregulated survivin gene expression, and induced caspase-9, -3 and -7 activities. Induction of apoptosis was associated with inhibition of survivin gene expression, and restoration of survivin levels remarkably attenuated β-elemene-induced glioma cell death. Moreover, we found that the interaction between surviving and HBXIP, a critical regulator of caspase-9 activity, was impaired by β-elemene treatment. The results, therefore, reveal a caspase-mediated apoptotic pathway induced by β-elemene in human glioma cells, which is associated with downregulation of survivin itself and the interaction between survivin and HBXP.
Insights
Beta-elemene from ginger induces cancer cell death by promoting apoptosis. This study reveals its mechanism involves downregulating survivin and affecting caspase activity in human glioma cells.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Beta-elemene, derived from ginger, exhibits antitumor properties in clinical settings.
- The precise mechanism of beta-elemene's cytotoxic effects, particularly in glioma, requires further elucidation.
Purpose of the Study:
- To investigate the molecular mechanisms by which beta-elemene induces cytotoxicity in human glioma cells.
- To explore the role of survivin and caspase activation in beta-elemene-mediated apoptosis.
Main Methods:
- Assessing beta-elemene's effect on apoptotic cell death in human glioma cells.
- Analyzing survivin gene expression and caspase-9, -3, and -7 activities.
- Investigating the interaction between survivin and HBXIP following beta-elemene treatment.
Main Results:
- Beta-elemene promoted apoptotic cell death in human glioma cells.
- Survivin gene expression was downregulated, and caspase-9, -3, and -7 activities were induced.
- Restoration of survivin levels attenuated beta-elemene-induced cell death.
- Beta-elemene impaired the interaction between survivin and HBXIP, a regulator of caspase-9 activity.
Conclusions:
- Beta-elemene induces apoptosis in human glioma cells via a caspase-mediated pathway.
- Downregulation of survivin and disruption of the survivin-HBXIP interaction are key events in beta-elemene's mechanism of action.
- These findings provide insights into the antitumor activity of beta-elemene and its potential therapeutic applications in glioma treatment.
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