Actein inhibits glioma growth via a mitochondria-mediated pathway
Abstract:
Previous studies indicate that the triterpene glycoside Actein from the herb black cohosh inhibits growth of human breast cancer cells. This study sought to investigate the effects of Actein on glioma cell growth and explore the potential mechanisms. Our results showed that administration of Actein significantly inhibited glioma cell viability in a dose- and time-dependent manner. Actein also increasingly inhibited the colony formation processes in glioma U87 cells and U251 cells. Administration of Actein also induced mitochondria-related apoptosis by increasing expression of pro-apoptotic factors Bax, cleaved caspase-3, cleaved caspase-9 and cleaved poly (ADP-ribose) polymerase 1 (PARP1) as well as decreasing anti-apoptotic Bcl-2 expression in U87 cells and U251 cells. In a xenograft model of glioma, Actein suppressed tumor growth and consistently induced cell apoptosis with the same mechanisms observed in vitro. In all, this study is the first report to address the growth inhibitory effects of Actein on glioma growth and propose that mitochondria-mediated apoptosis pathway may underlie the biological activities of Actein in glioma. Our study suggests that administration of Actein may serve as a potent therapeutic strategy for treatment of glioma.
Insights
Black cohosh triterpene glycoside Actein inhibits glioma cell growth and colony formation. Actein induces apoptosis via the mitochondria-mediated pathway, suggesting potential therapeutic use for glioma.
Area of Science:
- Pharmacology
- Cancer Biology
- Cell Biology
Background:
- Black cohosh (Actea racemosa) contains triterpene glycosides, including Actein.
- Previous research indicates Actein inhibits human breast cancer cell growth.
- Glioma is a primary brain tumor with limited treatment options.
Purpose of the Study:
- To investigate the anti-glioma effects of Actein.
- To explore the underlying mechanisms of Actein's action on glioma cells.
- To evaluate Actein's efficacy in a preclinical glioma model.
Main Methods:
- In vitro studies using U87 and U251 human glioma cell lines.
- Assessment of cell viability, colony formation, and apoptosis markers (Bax, Bcl-2, cleaved caspase-3, -9, PARP1).
- In vivo xenograft mouse model to assess tumor growth inhibition.
Main Results:
- Actein significantly inhibited glioma cell viability and colony formation in a dose- and time-dependent manner.
- Actein induced apoptosis in glioma cells by modulating pro-apoptotic (Bax, cleaved caspase-3, -9, PARP1) and anti-apoptotic (Bcl-2) factors.
- Actein suppressed tumor growth and induced apoptosis in a glioma xenograft model.
Conclusions:
- Actein exhibits significant growth inhibitory effects on glioma cells.
- Mitochondria-mediated apoptosis is a key mechanism underlying Actein's anti-glioma activity.
- Actein demonstrates potential as a therapeutic agent for glioma treatment.
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