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Isolation and Expansion of Human Glioblastoma Multiforme Tumor Cells Using the Neurosphere Assay
Published on: October 30, 2011
Activation of PPARγ mediates icaritin-induced cell cycle arrest and apoptosis in glioblastoma multiforme
Yongji Liu1, Ling Shi1, Yuan Liu1
1Department of Neurosurgery, The Affiliated Qingdao Hiser Hospital of Qingdao University (Qingdao Hospital of Traditional Chinese Medicine), Qingdao, Shandong, China.
Background:
Glioblastoma multiforme (GBM) is the most prevalent primary malignancy of the brain. This study was designed to investigate whether icaritin exerts anti-neoplastic activity against GBM in vitro.
Materials And Methods:
Cell Counting Kit-8 (CCK-8) assay was utilized to examine the viability of GBM cells. The apoptotic cell population was measured by flow cytometry analysis. Cell cycle distribution was detected by flow cytometry as well. Western blot analysis was performed to examine the level of biomarker proteins in GBM cells. Levels of PPARγ mRNA and protein were detected by qPCR and western blot analysis, respectively. To examine the role of PPARγ in the anti-neoplastic activity of icaritin, PPARγ antagonist GW9662 or PPARγ siRNA was used. The activity of PPARγ was determined by DNA binding and luciferase assays.
Results:
Our findings revealed that icaritin markedly suppresses cell growth in a dose-dependent and time-dependent fashion. The cell population at the G0/G1 phase of the cell cycle was significantly increased following icaritin treatment. Meanwhile, icaritin promoted apoptotic cell death in T98G and U87MG cells. Further investigation showed upregulation of PPARγ played a key role in the anti-neoplastic activities of icaritin. Moreover, our result demonstrated activation of AMPK signaling by icaritin mediated the modulatory effect of icaritin on PPARγ.
Conclusion:
Our results suggest the PPARγ may mediate anti-neoplastic activities against GBM.
Insights
Icaritin demonstrates anti-neoplastic effects against glioblastoma multiforme (GBM) by suppressing cell growth and promoting apoptosis. These effects are mediated by the upregulation of PPARγ and activation of AMPK signaling.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Glioblastoma multiforme (GBM) is the most common primary brain tumor.
- Investigating novel therapeutic agents for GBM is critical.
Purpose of the Study:
- To determine the in vitro anti-neoplastic activity of icaritin against GBM.
- To elucidate the underlying molecular mechanisms, including the role of PPARγ.
Main Methods:
- Cell Counting Kit-8 (CCK-8) assay for cell viability.
- Flow cytometry for apoptosis and cell cycle analysis.
- Western blot, qPCR, and luciferase assays for molecular targets (PPARγ, AMPK).
Main Results:
- Icaritin significantly suppressed GBM cell growth in a dose- and time-dependent manner.
- Icaritin induced cell cycle arrest at the G0/G1 phase and promoted apoptosis.
- Upregulation of PPARγ and activation of AMPK signaling were identified as key mechanisms.
Conclusions:
- PPARγ activation is implicated in the anti-neoplastic effects of icaritin on GBM.
- Icaritin shows potential as a therapeutic agent for GBM.
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