| 王克,范志刚,包志军.DHA对人脑胶质瘤T98G细胞迁移和侵袭的影响机制.[J].中南医学科学杂志.,2024,(2):182-186. |
| DHA对人脑胶质瘤T98G细胞迁移和侵袭的影响机制 |
| The mechanism of DHA's effect on the migration and invasion of human glioma T98G cells |
| 投稿时间：2022-12-22 修订日期：2024-02-22 |
| DOI：10.15972/j.cnki.43-1509/r.2024.02.006 |
| 中文关键词: 脑胶质瘤 双氢青蒿素 PI3K/Akt 黏附 迁移 侵袭 T98G细胞 [ |
| 英文关键词:glioma cancer DHA PI3K/Akt adhesion migration invasion T98G cells |
| 基金项目:陕西省科学技术厅2021年度科技计划项目(2021SF-044) |
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| 中文摘要: |
| 目的探究双氢青蒿素(DHA)对人脑胶质瘤T98G细胞迁移和侵袭的影响机制。 方法体外培养人脑胶质瘤T98G细胞,将其分为对照组、低DHA组(10 mg/L DHA)、中DHA组(20 mg/L DHA)、高DHA组(40 mg/L DHA)、阳性药物组(50 mg/L 5-氟尿嘧啶)和抑制剂组(20 mg/L DHA＋20 μmol/L LY294002)。采用CCK-8、细胞黏附实验、Transwell小室及蛋白免疫印迹法分别对细胞增殖活力、黏附、迁移、侵袭能力及上皮间质转化(EMT)、磷脂酰肌醇3-激酶(PI3K)/丝苏氨酸蛋白激酶(Akt)通路相关蛋白的表达水平进行分析。 结果随着细胞处理时间的递增,各组T98G细胞增殖活力呈递增趋势(P＜0.05)。与对照组比较,其他各组T98G细胞增殖活力、黏附、迁移和侵袭能力、p-PI3K、p-Akt、p-ERK、N-cadherin、Vimentin和FN蛋白表达均显著降低(P＜0.05),而E-cadherin蛋白表达显著升高(P＜0.05),且低、中、高DHA组呈剂量依赖性降低或升高(P＜0.05)。与低、中DHA组比较,阳性药物组、抑制剂组细胞增殖活力、黏附、迁移和侵袭能力、p-PI3K、p-Akt、p-ERK、N-cadherin、Vimentin和FN蛋白显著降低(P＜0.05),而E-cadherin蛋白表达显著升高(P＜0.05)。 结论DHA抑制人脑胶质瘤T98G细胞的黏附、迁移、侵袭和EMT,其机制可能是通过抑制PI3K/Akt通路的信号转导发挥作用。 |
| 英文摘要: |
| AimTo investigate the mechanism of the effects of dihydroartemisinin (DHA) on migration and invasion of human glioma T98G cells. MethodsHuman glioma T98G cells were cultured in vitro, and were divided into control group, low DHA group (10 mg/L DHA), medium DHA group (20 mg/L DHA), high DHA group (40 mg/L DHA), positive drug group (50 mg/L 5-fluorouracil) and inhibitor group (20 mg/L DHA+20 μmol/L LY294002). CCK-8, cell adhesion assay, Transwell chamber and Western blotting were used to analyze cell proliferation, adhesion, migration, invasion, EMT and phosphatidylinositol 3-kinase (PI3K)/seronine protein kinase (Akt) path-related protein expression levels in each group, respectively. ResultsWith the cell processing time increased, the proliferation activity of T98G cells in each group showed a trend of increase (P＜0.05). Compared with the control group, the proliferation activity, adhesion, migration and invasion ability, and the expression of p-PI3K, p-Akt, p-ERK, N-cadherin, Vimentin, and FN protein of T98G cells in other groups were significantly decreased (P＜0.05),while the expression of E-cadherin protein is significantly increased (P＜0.05), and the low, medium, and high DHA groups showed a dose-dependent decrease or increase (P＜0.05). Compared with the low and medium DHA groups, the proliferation activity, adhesion, migration and invasion ability, and the expression of p-PI3K, p-Akt, p-ERK, N-cadherin, Vimentin, and FN protein of T98G cells in the positive drug group and inhibitor group were significantly decreased (P＜0.05), while the expression of E-cadherin protein was significantly increased (P＜0.05). ConclusionDHA inhibits adhesion, migration, invasion and EMT of human glioma T98G cells, possibly by inhibiting the signal transduction of PI3K/Akt pathway. |
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