Chidamide Inhibits Glioma Cells by Increasing Oxidative Stress via the miRNA-338-5p Regulation of Hedgehog Signaling
Joint Authors
Zhou, Haixia
Han, Liang
Wang, Han
Wei, Jun
Guo, Zhigang
Li, Zhaohui
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-17, 17 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-03-11
Country of Publication
Egypt
No. of Pages
17
Main Subjects
Abstract EN
Objective.
Chidamide has a broad spectrum of antitumor activity but its function on glioma remains unknown.
The increase of reactive oxygen species (ROS) and reactive nitrogen species (RNS) may control glioma risk by promoting its apoptosis and necrosis.
Hedgehog pathway is crucial to glioma cell proliferation and controls ROS production.
We aimed to explore the effects of chidamide on the levels of miR-338-5p (glioma cell inhibitor), which may regulate Hedgehog signaling, resulting in the changes of RNS.
Materials and Methods.
Migration and invasion activities of glioma cells were measured by using the Transwell chamber assay.
The expression levels of Sonic Hedgehog (Shh), Indian Hedgehog (Ihh), Desert Hedgehog (Dhh), miR-338-5p, and related molecules were detected by using real-time PCR (RT-PCR) and or Western Blot in U87 and HS683 glioma cells.
The effects of chidamide on these molecules were measured by using the miR-338-5p inhibitor or mimics in U87 and HS683 glioma cell lines.
ROS and RNS were measured by DCF DA and DAF-FM DA fluorescence.
Biomarkers of oxidative stress were measured by using a corresponding kit.
Apoptosis and necrosis rates were measured by using flow cytometry.
Results.
Chidamide inhibited the growth rate, migration, and invasion of human malignant glioma cells and increased the level of miR-338-5p.
miR-338-5p inhibitor or mimics increased or inhibited the growth rate of U87 and HS683 glioma cells.
Chidamide inhibited the levels of Shh, Ihh, migration protein E-cadherin, and invading protein MMP-2.
The increase in the level of Shh and Ihh led to the reduction in the ROS and RNS levels.
miR-338-5p inhibitor or mimics also showed a promoting or inhibitory function for the levels of Shh and Ihh.
Furthermore, miR-338-5p mimics and inhibitor inhibited or promoted the migration and invasion of the glioma cells (P<0.05).
Evaluated levels of miR-338-5p increased oxidative stress level and apoptosis and necrosis rate by regulating the levels of biomarkers of oxidative stress (P<0.05).
Conclusion.
Chidamide inhibits glioma cells by increasing oxidative stress via the miRNA-338-5p regulation of Hedgehog signaling.
Chidamide may be a potential drug in the prevention of glioma development.
American Psychological Association (APA)
Zhou, Haixia& Han, Liang& Wang, Han& Wei, Jun& Guo, Zhigang& Li, Zhaohui. 2020. Chidamide Inhibits Glioma Cells by Increasing Oxidative Stress via the miRNA-338-5p Regulation of Hedgehog Signaling. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-17.
https://search.emarefa.net/detail/BIM-1205292
Modern Language Association (MLA)
Zhou, Haixia…[et al.]. Chidamide Inhibits Glioma Cells by Increasing Oxidative Stress via the miRNA-338-5p Regulation of Hedgehog Signaling. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-17.
https://search.emarefa.net/detail/BIM-1205292
American Medical Association (AMA)
Zhou, Haixia& Han, Liang& Wang, Han& Wei, Jun& Guo, Zhigang& Li, Zhaohui. Chidamide Inhibits Glioma Cells by Increasing Oxidative Stress via the miRNA-338-5p Regulation of Hedgehog Signaling. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-17.
https://search.emarefa.net/detail/BIM-1205292
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1205292