Abstract
Fraxetin (FXT) exerts anticancer function in multiple cancers, but its function on glioma was ill-defined. This article expounded the mechanism by which FXT exerts an anticancer effect in glioma. The effect of gradient concentration of FXT on the viability of glioma cell lines was determined by cell counting kit 8. Effects of FXT on proliferation, apoptosis, and cell cycle in glioma cell lines were determined by colony formation assay, flow cytometry, and Hoechst 33342 staining. Expressions of apoptosis-related gene, cycle-related gene, and glioma-related miRNAs after FXT (25 and 50 μmol/L) treatment were determined by quantitative reverse transcription polymerase chain reaction and western blot as needed. After miR-21-3p overexpression, cell viability and apoptosis of glioma cell lines treated with FXT (50 μmol/L) were tested again. Although 1 μmol/L FXT had no significant effect on cell viability, 5, 10, 25, and 50 μmol/L FXT suppressed cell viability in a concentration-dependent manner. FXT inhibited proliferation, promoted apoptosis, and induced cell cycle arrest in G0/G1 phase in glioma cell lines. These effects may be achieved by elevated expressions of Bax and cleaved caspase-3 and diminished expressions of Bcl-2, Bcl-XL, cyclin E1, cyclin D1, and cyclin-dependent kinase-6. FXT attenuated the contents of miR-21-3p and miR-455-3p, and escalated the contents of miR-124-3p and miR-7-5p. The regulation of FXT on cell viability, proliferation and apoptosis was reversed by miR-21-3p overexpression. FXT suppressed the development of glioma cells by downregulating miR-21-3p.