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Ginsenoside Rh2 inhibits metastasis of glioblastoma multiforme through Akt-regulated MMP13
Ning Guan1, Xiaochuan Huo1, Zhenxing Zhang1
1Department of Neurosurgery, The First Affiliated Hospital of Liaoning Medical University, 2 Renmin Road, Jinzhou, 121001, China.
Abstract:
Glioblastoma multiforme (GBM) is the most malignant type of primary brain tumor. Although the growth of the tumor cells in a relatively closed space may partially account for its malignancy, highly invasive nature of glioblastoma cells has been suggested to be the main reason for the failure of current therapeutic approaches. Ginsenoside Rh2 (GRh2) has recently been shown to significantly suppress the growth and survival of GBM through inhibiting epidermal growth factor receptor signaling, whereas its effects on the invasion and metastasis have not been examined. Here, we showed that GRh2 dose-dependently decreased GBM cell invasiveness in both scratch wound healing assay and Transwell cell migration assay. Moreover, the inhibitory effects of GRh2 on cell migration seemed to be conducted through decreased expression of matrix metalloproteinase (MMP)-13. Furthermore, using specific inhibitors, we found that GRh2 inhibited MMP13 through PI3k/Akt signaling pathway. Finally, high MMP13 levels were detected in GBM specimen from the patients. Together, these data suggest that GRh2 may suppress GBM migration through inhibiting Akt-mediated MMP13 activation. Thus, our data highlight a previous unappreciated role for GRh2 in suppressing GBM cell metastasis.
Insights
Ginsenoside Rh2 (GRh2) reduces glioblastoma multiforme (GBM) cell invasion by decreasing matrix metalloproteinase-13 (MMP13) expression via the PI3k/Akt pathway. This study reveals GRh2
Area of Science:
- Neuro-oncology
- Cancer biology
- Pharmacology
Background:
- Glioblastoma multiforme (GBM) is an aggressive primary brain tumor.
- The invasive nature of GBM cells contributes to therapeutic failure.
- Ginsenoside Rh2 (GRh2) inhibits GBM growth but its anti-metastatic effects are unknown.
Purpose of the Study:
- To investigate the effects of GRh2 on GBM cell invasion and metastasis.
- To elucidate the molecular mechanisms underlying GRh2's anti-invasive action.
- To assess the relevance of these findings in patient GBM specimens.
Main Methods:
- Scratch wound healing and Transwell cell migration assays were used to assess GBM cell invasiveness.
- Matrix metalloproteinase-13 (MMP13) expression levels were analyzed.
- PI3k/Akt signaling pathway was investigated using specific inhibitors.
- GBM patient specimens were analyzed for MMP13 levels.
Main Results:
- GRh2 dose-dependently inhibited GBM cell invasiveness and migration.
- GRh2 decreased MMP13 expression, a key factor in cell migration.
- GRh2's anti-migratory effect was mediated through the PI3k/Akt signaling pathway.
- Elevated MMP13 levels were observed in GBM patient samples.
Conclusions:
- GRh2 suppresses GBM cell migration and invasion.
- The mechanism involves the inhibition of Akt-mediated MMP13 activation.
- GRh2 shows potential as a therapeutic agent against GBM metastasis.
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