Amentoflavone induces apoptosis and suppresses glycolysis in glioma cells by targeting miR-124-3p

• Published in: Neuroscience letters Vol. 686; pp. 1 - 9
• Main Authors: Zhaohui, Wang, Yingli, Niu, Hongli, Lin, Haijing, Wang, Xiaohua, Zhang, Chao, Fang, Liugeng, Wu, Hui, Zhang, Feng, Tian, Linfeng, Yang, Hong, Jiang
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 01.11.2018
• Subjects: Amentoflavone; Apoptosis; DNMT1; Glioma; Glycolysis; miR-124-3p; Amentoflavone; Glycolysis; DNMT1; miR-124-3p; Glioma; Apoptosis
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2018.08.032

[Display omitted] •AF suppressed glioma cells.•AF induced apoptosis and inhibited glycolysis.•AF upregulated miR-124-3p by repressing DNMT1 through Sp1, which caused by activation of ROS/AMPK. Malignant glioma is the most common type of brain tumor with poor clinical outcome and survival. Therefore, it is imperative to develop novel therapeutic agents for managing glioma. The aim of this study was to investigate the role of amentoflavone (AF), an active flavonoid component in Selaginella tamariscina Spring, in glioma cells and the underlying mechanism of its action. Our results showed that miR-124-3p expression was significantly down-regulated in glioma tissues relative to normal brain tissues. AF decreased cell viability and triggered apoptosis in both glioma cell lines in a dose-dependent manner. AF induced apoptosis and inhibited glycolysis in the glioma cells by upregulating miR-124-3p. Furthermore, AF upregulated miR-124-3p by repressing DNMT1 through Sp1, which in turn was caused by the activation of ROS/AMPK signaling pathway by AF. In conclusion, AF could induce apoptosis and inhibited glycolysis in glioma cells via miR-124-3p. Our findings provide preliminary experimental data that support further investigation on the therapeutic efficacy of AF in glioma.