Effects of Butorphanol on Proliferation Migration and Angiogenesis of Lung Cancer Cells by Regulating the Wnt/β-Catenin Signaling Pathway
Objective:To investigate the effects of buprenorphine on the proliferation,migration,and angiogenesis of lung cancer cells by regulating the Wnt/β-catenin signaling pathway.Methods:Human lung cancer H1299 cells were divided into the control group,low-dose and high-dose buprenorphine groups,high-dose buprenorphine+LiCl(Wnt/β-catenin signaling pathway activator)group,and FH535 group(Wnt/β-catenin signaling pathway inhibitor).The colony formation assay was used to detect the colony formation a-bility of cells;the Transwell assay was used to detect cell migration and invasion;flow cytometry was used to detect the cell apoptosis rate;the vascular mimicry formation assay was used to observe the angiogenesis;and Western blot was used to detect the expression of VEGF-A,VE-cadherin,Bcl-2,Bax,MMP-9,β-cate-nin,c-Myc,and cyclin D1 proteins.Results:The lumen structure of H1299 cells in the control group was in-tact;compared with the control group,the clone formation rate of H1299 cells,the numbers of cell migration and invasion,number of lumens,and the expression of VEGF-A,VE cadherin,Bcl-2,MMP-9,β-cate-nin,c-Myc,and cyclin D1 proteins were greatly reduced in the low-dose butorphanol group,high-dose bu-torphanol group,and FH535 group,the apoptosis rate and the expression of Bax protein were greatly increased(P<0.05);LiCl was able to partially reverse the inhibitory effect of butorphanol on the malignant biological behavior of H1299 cells(P<0.05);the various detection indicators of H1299 cells in the FH535 group were at the same level as those in the high-dose Butorphanol group(P<0.05).Conclusion:Butorphanol can in-duce apoptosis of lung cancer cells,block migration,proliferation and vascular growth,and then prevent the occurrence and development of lung cancer.The mechanism is related to blocking the activation of Wnt/β-catenin signaling pathway.
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