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Research Paper|Volume 15, Issue 18|pp 9377—9390

Ar-turmerone inhibits the proliferation and mobility of glioma by downregulating cathepsin B

Wenpeng Cao1, Xiaozhong Chen2, Chaolun Xiao1, Dengxiao Lin1, Yumei Li1, Shipeng Luo1, Zhirui Zeng3, Baofei Sun1, Shan Lei3
  • 1Department of Anatomy, Key Laboratory of Human Brain Bank for Functions and Diseases of Department of Education of Guizhou Province, Guizhou Medical University, Guiyang 550009, Guizhou, China
  • 2Department of Neurosurgery, The Jinyang Hospital Affiliated to Guizhou Medical University, Guiyang 550009, Guizhou, China
  • 3Department of Physiology, School of Basic Medicine, Guizhou Medical University, Guiyang 550009, Guizhou, China
* Equal contribution
Received: May 2, 2023Accepted: July 18, 2023Published: September 26, 2023

Copyright: © 2023 Cao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Ar-turmerone, a compound isolated from turmeric seeds, has exhibited anti-malignant, anti-aging and anti-inflammatory properties. Here, we assessed the effects of ar-turmerone on glioma cells. U251, U87 and LN229 glioma cell lines were treated with different concentrations of ar-turmerone (0, 50, 100 and 200 μM), and their viability and mobility were evaluated using Cell Counting Kit 8, colony formation, wound healing and Transwell assays. The effects of ar-turmerone on U251 glioma cell proliferation were also assessed using a subcutaneous implantation tumor model. High-throughput sequencing, bioinformatic analyses and quantitative real-time polymerase chain reactions were used to identify the key signaling pathways and targets of ar-turmerone. Ar-turmerone reduced the proliferation rate and mobility of glioma cells in vitro and arrested cell division at G1/S phase. Cathepsin B was identified as a key target of ar-turmerone in glioma cells. Ar-turmerone treatment reduced cathepsin B expression and inhibited the cleavage of its target protein P27 in glioma cells. On the other hand, cathepsin B overexpression reversed the inhibitory effects of ar-turmerone on glioma cell proliferation, mobility progression in vitro and in vivo. In conclusion, ar-turmerone suppressed cathepsin B expression and P27 cleavage, thereby inhibiting the proliferation and mobility of glioma cells.