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

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.

FOXP3 promote the progression of glioblastoma via inhibiting ferroptosis mediated by linc00857/miR-1290/GPX4 axis

“…Ferroptosis, a form of RCD dependent on iron and controlled by GPX4, is primarily initiated by severe lipid peroxidation resulting from the generation of ROS and the availability of iron [ 18 ]. A growing body of evidence indicates the significant involvement of ferroptosis in GBM progression, with several drugs demonstrating anti-tumor effects and synergistic effects with temozolomide by targeting regulatory molecules associated with ferroptosis in glioma, especially in GBM [ 19 , 20 ]. Therefore, the identification of these regulatory molecules holds potential for enhancing GBM therapy.…”