Biological mechanism of bafilomycin A1 inhibiting glioma migration,invasion and vasculogenicmimicry

doi:10.19854/j.cnki.1008-2425.2022.02.0003

Abstract

Abstract: Objective To study the effect of Baflomycin A1 (BAF-A1) on glioma cell proliferation,invasion and migration and vasculogenic mimicry (vm) and its mechanism of action. Methods ①After glioma cell lines U87 and U251 were treated with pavlomycin A1 (10 nmol / ml),the activity of vacuolar ATPase (V-ATPase) and the pH value of culture medium were detected,and the cell proliferation of each group was detected by CCK-8 method.②Three dimensional culture technique and Transwell chamber were used to observe the VM formation state and invasion ability of cells in each group.③Western blot was used to explore the expression level of PI3K / Akt in cells of each group. Results ① Compared with the control group,the V-ATPase of U87 and U251 cells after treatment with bafilomycin A1,The activity was inhibited (P＜0.05);thePH value of the extracellular culture medium was increased (P＜0.05);the proliferation and migration of cells were inhibited (P＜0.05);the mimic ability of angiogenesis was weakened (P＜0.05).② Compared with the control group,the expression levels of PI3K and AKT proteins in U87 and U251 cells were significantly decreased after treatment with bafilomycin A1 (P＜0.05). Conclusion Bafilomycin A1 alters tumor migration,invasion and angiogenesis mimicry by inhibiting the activity of V-ATPase,which may be related to PI3K/AKT and other related signaling pathways.

Key words: Bafilomycin A1, Glioma, Invasion, Vasculogenic mimicry

摘要： 目的研究巴佛洛霉素A1(Baflomycin A1,BAF-A1)对胶质瘤细胞增殖、侵袭迁移和血管生成拟态(vasculogenic mimicry,vm)的影响及其作用机制探讨。方法 ①利用巴佛洛霉素 A1(10 nmol/mL)处理胶质瘤细胞系U87和U251后,检测各组液泡-ATP酶(vacular-ATPases,V-ATPases)活性及培养液PH值,利用CCK-8法检测各组细胞增殖情况。②利用三维培养技术和Transwell小室观察各组细胞VM形成状态和侵袭能力。③采用western-blot法探究各组细胞中PI3K/AKT的表达水平。结果 ①与对照组相比,使用巴佛洛霉素 A1处理后,U87和U251细胞的 V-ATPase活性受到抑制(P＜0.05);细胞外培养液的PH值升高(P＜0.05);细胞的增殖和迁移能力被抑制(P＜0.05);血管生成拟态能力减弱(P＜0.05)。②与对照组相比,使用巴佛洛霉素 A1处理后,U87和U251细胞的PI3K、AKT蛋白的表达水平均显著降低(P＜0.05)。结论巴佛洛霉素A1通过抑制V-ATPase的活性来改变肿瘤的迁移、侵袭和血管生成拟态,其可能与PI3K/AKT等相关信号通路相关。

关键词: 巴佛洛霉素 A1, 胶质瘤, 侵袭, 血管生成拟态

CLC Number:

R739.41

Chen Fenglong, Chen Jinjong, Zhang Yi. Biological mechanism of bafilomycin A1 inhibiting glioma migration,invasion and vasculogenicmimicry[J]. Chinese Journal of Stereotactic and Functional Neurosurgery, 2022, 35(2): 75-80.

陈锋龙, 陈金龙, 张弋. 巴佛洛霉素A1抑制胶质瘤迁移、侵袭及血管生成拟态的生物机制研究[J]. 立体定向和功能性神经外科杂志, 2022, 35(2): 75-80.

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