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Published on: April 26, 2018
Fraxetin exerts anticancer effect in glioma by suppressing MiR-21-3p
Hanxun Yao1, Xiaobin Li1, Xuyan Pan1
1Department of Neurosurgery, Huzhou Central Hospital, Huzhou, China.
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.
Insights
Fraxetin (FXT) inhibits glioma cell growth by reducing proliferation and inducing apoptosis. This anticancer effect is mediated by regulating specific genes and downregulating miR-21-3p.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Fraxetin (FXT) demonstrates anticancer properties across various cancers, but its specific role in glioma remains unclear.
- Glioma is a challenging brain tumor with limited effective therapeutic options.
Purpose of the Study:
- To elucidate the mechanism by which Fraxetin (FXT) exerts anticancer effects on glioma cells.
- To investigate the impact of FXT on glioma cell viability, proliferation, apoptosis, and cell cycle.
- To explore the role of specific microRNAs (miRNAs) in mediating FXT's anti-glioma activity.
Main Methods:
- Cell counting kit-8 (CCK-8) assay to assess cell viability.
- Colony formation assay, flow cytometry, and Hoechst 33342 staining to evaluate proliferation, apoptosis, and cell cycle.
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot to analyze gene and miRNA expression.
- MiR-21-3p mimic transfection to confirm its role in FXT's mechanism.
Main Results:
- FXT suppressed glioma cell viability, proliferation, and induced G0/G1 cell cycle arrest in a dose-dependent manner.
- FXT altered the expression of apoptosis-related genes (Bax, cleaved caspase-3, Bcl-2, Bcl-XL) and cell cycle regulators (cyclin E1, cyclin D1, CDK6).
- FXT modulated glioma-associated miRNAs, decreasing miR-21-3p and miR-455-3p while increasing miR-124-3p and miR-7-5p.
- Overexpression of miR-21-3p reversed the effects of FXT on cell viability, proliferation, and apoptosis, confirming its regulatory role.
Conclusions:
- Fraxetin exhibits significant anti-glioma potential by inhibiting cell proliferation, promoting apoptosis, and inducing cell cycle arrest.
- FXT exerts its effects, at least in part, by modulating the expression of key apoptosis and cell cycle regulatory genes.
- Downregulation of miR-21-3p is a critical mechanism through which Fraxetin suppresses glioma cell development.
