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| Effects of Butorphanol on Proliferation Migration and Angiogenesis of Lung Cancer Cells by Regulating the Wnt/β-Catenin Signaling Pathway |
| WEN Zhu, et al |
| Mianyang Central Hospital, Sichuan Mianyang 621000, China |
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Abstract 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 ability 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-catenin, c-Myc, and cyclin D1 proteins. Results: The lumen structure of H1299 cells in the control group was intact; 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-catenin, c-Myc, and cyclin D1 proteins were greatly reduced in the low-dose butorphanol group, high-dose butorphanol 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 induce 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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2024, Vol. 30 
