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ScienceAsia (): 786-790 |doi: 10.2306/scienceasia1513-1874..072


Atractylenolide-II inhibits proliferation and migration of glioblastoma cells


Rui Wanga,b,?, Tingting Liuc,?, Jiayu Chena,b, Dianbao Zhanga,b,*

 
ABSTRACT:     Glioblastoma (GBM) is the most malignant and lethal brain tumor in adults, with limited therapeutic options and dismal prognosis. Atractylenolide-II (AT-II) is a major bioactive compound from Atractylodes macrocephala Koidz. (Baizhu in Chinese), with anti-inflammatory and anti-tumor activities. However, the anti-tumor effects of AT-II on GBM cells remain unclear. In the present study, the cytotoxicity of AT-II on GBM cells was analyzed using CCK-8 assay, and it revealed that the cell viability was inhibited by AT-II in a dose-dependent manner. The results of Transwell migration assay indicated that AT-II treatment significantly inhibited the cell migration. Furthermore, the cell cycle arrest at G0/G1 phase in AT-II treated cells was presented in the flow cytometry data. Consistently, real-time PCR and western blotting revealed a remarkable decrease of the CCNA and CCNB expression upon AT-II treatment. Moreover, the phosphorylation of both extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) was triggered by AT-II. Collectively, these results suggested that MAPK signaling was involved in AT-II induced cell cycle arrest, contributing to the inhibition of cell viability and migration of GBM cells.

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a Department of Stem Cells and Regenerative Medicine, Key Laboratory of Cell Biology, National Health Commission of China, China Medical University, Shenyang 110122 China
b Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122 China
c Department of Food and Drug, Liaoning Agricultural Technical College, Yingkou 115009 China

* Corresponding author, E-mail: zhangdianbao@gmail.com

Received 13 Aug 2022, Accepted 26 Jul 2023