Conclusions
FOXM1 may promote malignant meningioma via the AHR signaling pathway, which improved the current understanding of the role of FOXM1 in meningioma.
Material and methods
Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect FOXM1 expression in malignant meningioma and adjacent tissues. The viability, proliferation, apoptosis and tube formation of meningioma IOMM-Lee and CH157-MN cells transfected with overexpressed FOXM1 were examined with MTT assay, clone formation assay, flow cytometry and tube formation assay, respectively. The expressions of AHR and cytochrome P450 family 1 subfamily A member 1 (CYP1A1) in meningioma and adjacent tissues were detected using qRT-PCR, and the correlation of AHR with FOXM1 was analyzed with Pearson's correlation analysis. Western blot was conducted for measuring the expressions of vascular endothelial growth factor A (VEGFA), AHR and CYP1A1. The cell viability, proliferation, apoptosis and tube formation capability were further determined after treatment with StemRegenin 1 (SR1) (an AHR signaling pathway inhibitor), and transfected with or without overexpressed FOXM1.
Methods
Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect FOXM1 expression in malignant meningioma and adjacent tissues. The viability, proliferation, apoptosis and tube formation of meningioma IOMM-Lee and CH157-MN cells transfected with overexpressed FOXM1 were examined with MTT assay, clone formation assay, flow cytometry and tube formation assay, respectively. The expressions of AHR and cytochrome P450 family 1 subfamily A member 1 (CYP1A1) in meningioma and adjacent tissues were detected using qRT-PCR, and the correlation of AHR with FOXM1 was analyzed with Pearson's correlation analysis. Western blot was conducted for measuring the expressions of vascular endothelial growth factor A (VEGFA), AHR and CYP1A1. The cell viability, proliferation, apoptosis and tube formation capability were further determined after treatment with StemRegenin 1 (SR1) (an AHR signaling pathway inhibitor), and transfected with or without overexpressed FOXM1.
Results
FOXM1, AHR and CYP1A1 expressions were upregulated in malignant meningioma tissues. Overexpressed FOXM1 promoted meningioma cell viability, proliferation, tube formation, upregulated expressions of AHR, CYP1A1 and VEGFA, and inhibited the cell apoptosis. AHR was positively correlated with FOXM1. SR1 suppressed meningioma cell growth and the AHR signaling pathway, and also reversed the active effect of FOXM1 on meningioma cells. Conclusions: FOXM1 may promote malignant meningioma via the AHR signaling pathway, which improved the current understanding of the role of FOXM1 in meningioma.