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Biomed Pharmacother. 2018 Apr;100:358-366. doi: 10.1016/j.biopha.2018.02.006. Epub 2018 Feb 16.

Activation of PPARγ mediates icaritin-induced cell cycle arrest and apoptosis in glioblastoma multiforme.

Author information

1
Department of Neurosurgery, The Affiliated Qingdao Hiser Hospital of Qingdao University (Qingdao Hospital of Traditional Chinese Medicine), Qingdao, Shandong, China. Electronic address: dryongjiliu@163.com.
2
Department of Neurosurgery, The Affiliated Qingdao Hiser Hospital of Qingdao University (Qingdao Hospital of Traditional Chinese Medicine), Qingdao, Shandong, China.
3
Department of Emergency, The Affiliated Qingdao Hiser Hospital of Qingdao University (Qingdao Hospital of Traditional Chinese Medicine), Qingdao, Shandong, China.
4
Department of Radiology, The Affiliated Qingdao Hiser Hospital of Qingdao University (Qingdao Hospital of Traditional Chinese Medicine), Qingdao, Shandong, China.
5
Department of Rheumatology and Immunology, The Affiliated Qingdao Hiser Hospital of Qingdao University (Qingdao Hospital of Traditional Chinese Medicine), Qingdao, Shandong, China.
6
Department of Neurology, Linyi People's Hospital, Linyi, Shandong, China.
7
Department of Oncology, Qingdao Central Hospital, Qingdao, Shandong, China. Electronic address: jufangjufang@sina.com.

Abstract

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.

KEYWORDS:

AMPK; GBM; Icaritin; PPARγ

PMID:
29453045
DOI:
10.1016/j.biopha.2018.02.006
[Indexed for MEDLINE]

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