Impacts of Butorphanol on the proliferation,migration and angiogenesis of cervical cancer cells by regulating hypoxia-inducible factor-1α/vascular endothelial growth factor signaling pathway
Objective To investigate the impacts and mechanism of Butorphanol on the proliferation,migration and angiogenesis of cervical cancer cells.Methods HeLa cells were treated with 0.5-80.0 μg/mL Butorphanol for 24h respectively.Cell proliferation was detected by cell counting kit-8(CCK-8)method,and half maximal inhibitory concentration(IC50)value was calculated.HeLa cells were grouped into control group,negative control group(NC group),hypoxia-inducible factor-1α(HIF-1α)overexpression group(HIF-1αgroup),Butorphanol group,and Butorphanol+HIF-1α group.The proliferation,migration,invasion and angiogenesis of HeLa cells were detected by plate cloning test,cell scratch test,Transwell cell test and tubule formation test.Western blot was applied to detect the protein expression of HIF-1α and vascular endothelial growth factor(VEGF),and the effect of Butorphanol on the growth of cervical cancer transplanted tumor was tested in nude mice.Results Overexpression of HIF-1α obviously promoted the proliferation,migration,invasion and angiogenesis mimicry of HeLa cells,and up-regulated the expression of HIF-1α and VEGF protein(P＜0.05).Butorphanol was able to effectively inhibit the proliferation,migration,invasion,angiogenesis mimicry formation of HeLa cells and the growth of cervical cancer transplanted tumor,and down-regulate the protein expression of HIF-1α and VEGF(P＜0.05).The inhibitory effect of Butorphanol on cervical cancer cells was able to be weakened by the overexpression of HIF-1α.Conclusions Butorphanol can inhibit the proliferation,migration,invasion and angiogenesis of cervical cancer cells and inhibit the growth of cervical cancer by inhibiting HIF-1α/VEGF signal pathway.
ButorphanolHypoxia-inducible factor-1 α/vascular endothelial growth factor signal pathwayCervical cancer cellsProliferationMigrationAngiogenic mimicry
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