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Archive > Volume 31 Issue 8 > 2024,31(8):796-802. DOI:10.3872/j.issn.1007-385X.2024.08.007 Prev Next
Basic Research
Astilbin inhibits proliferation, migration and vasculogenic mimicry formation of breast cancer cells by regulating HIF-1α/VEGF axis
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Abstract:
Objective: To explore the effects of astilbin (AST) on the proliferation, migration and vasculogenic mimicry (VM) formation in breast cancer cells by regulating the hypoxia-inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) axis. Methods: Breast cancer cells (MCF-7 and MDA-MB-231) were treated with AST at different concentrations (0, 5, 25, 50, 100, 150, 200, 300 μmol/L), and the cell viability was detected using the CKK-8 assay. The MCF-7 and MDA-MB-231 cells were divided into control group, low-dose AST (AST-L), medium-dose AST (AST-M), high-dose AST (AST-H), and AST-H+DMOG (HIF-1α/VEGF pathway activator) groups. The effect of AST on cell proliferation was detected by EdU assay, the influence on apoptosis was detected using flow cytometry, the migration and invasion abilities of cells were examined using Transwell chamber assay, and the VM formation was analyzed using Matrigel tube formation assay. The expression of HIF-1α, VEGF, VE-cadherin, E-cadherin, N-cadherin and MMP-2 was detected by WB assay. Results: Compared with 0 μmol/L AST, the viability of cells treated with 5, 25, 50, 100, 150, 200, and 300 μmol/L AST decreased obviously, which was in a dose-dependent manner (P protein expression of HIF-1α, VEGF, VE-cadherin, N-cadherin, and MMP-2, while the apoptosis rate and E-cadherin protein expression obviously increased (all PPConclusion: AST can inhibit the proliferation, migration, invasion, and VM formation of breast cancer cells and promote apoptosis, which may be related to the inhibition of the HIF-1α/VEGF signaling pathway.
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