出 处:《中国临床药理学杂志》2023年第20期2937-2941,共5页The Chinese Journal of Clinical Pharmacology
基 金:浙江省自然科学基金资助项目(LY17H140001)。
摘 要:目的 探究丹参酮ⅡA对口腔鳞状细胞癌(OSCC)SCC15细胞生物学行为和磷脂酰肌醇3激酶/磷酸化蛋白激酶B(PI3K/AKT)信号通路的影响。方法 将SCC15细胞分为对照组和实验1、2、3、4组,分别加入DMSO和2.5、5、10、20 mg·L^(-1)丹参酮ⅡA进行处理。用四甲基偶氮唑盐(MTT)法检测细胞生长抑制率;用克隆形成试验检测细胞克隆形成率;用流式细胞仪及Annexin V/PI染色法分析细胞凋亡率;用Transwell试验分析细胞迁移和侵袭能力;用蛋白质印迹法检测细胞磷酸化PI3K(p-PI3K)、磷酸化AKT(p-AKT)蛋白表达水平。结果 对照组和实验1、2、3、4组细胞克隆形成率分别为(167.71±20.73)%、(113.42±14.60)%、(78.57±15.08)%、(49.14±5.33%)和(22.57±4.43)%;细胞凋亡率分别为(8.43±1.28)%、(17.46±1.65)%、(31.92±5.39)%、(49.98±7.47)%和(83.69±5.94)%;迁移细胞数分别为(151.33±15.36)、(118.67±18.53)、(81.67±9.51)、(68.33±4.18)和(26.33±2.09)个;侵袭细胞数分别为(82.67±9.15)、(74.33±6.34)、(36.33±3.32)、(20.67±2.26)和(13.67±0.89)个;p-PI3K蛋白相对表达水平分别为0.92±0.11、0.80±0.12、0.61±0.07、0.42±0.05和0.15±0.03;p-AKT蛋白相对表达水平分别为1.21±0.14、0.73±0.12、0.59±0.11、0.49±0.09和0.27±0.05。各实验组与对照组比较,差异均有统计学意义(均P<0.05),且各实验组间呈剂量依赖性(均P<0.05)。结论 丹参酮ⅡA可抑制OSCC细胞生长、克隆、迁移和侵袭,促进细胞凋亡,可能通过抑制PI3K/AKT信号通路发挥抗癌作用。Objective To explore the effect of tanshinoneⅡA on the biological behavior and PI3K-AKT signaling pathway of oral squamous cell carcinoma (OSCC) SCC15 cells.Methods SCC15 cells were divided into control group and experimental-1,-2,-3 and-4groups,and they were given DMSO and 2.5,5,10,20 mg·L^(-1)tanshinoneⅡA for treatment respectively.The growth inhibition rate of SCC15 cells was detected by methyl thiazolyl tetrazolium (MTT) assay,and the clone formation rate was detected by clone formation assay.The cell apoptosis rate was analyzed by flow cytometry and Annexin V/PI staining,and the cell migration and invasion were analyzed by Transwell assay.Western blot assay was used to detect the protein expression levels of phosphorylated phosphatidylinositol 3 kinase (p-PI3K) and phosphorated protein kinase B (p-AKT).ResultsThe clone formation rates in control group and experimental-1,-2,-3 and-4 groups were (167.71±20.73)%,(113.42±14.60)%,(78.57±15.08)%,(49.14±5.33)%and (22.57±4.43)%;the cell apoptosis rates were(8.43±1.28)%,(17.46±1.65)%,(31.92±5.39)%,(49.98±7.47)%and (83.69±5.94)%;the migrating cell counts were (151.33±15.36),(118.67±18.53),(81.67±9.51),(68.33±4.18) and(26.33±2.09) cells;the invasive cell counts were (82.67±9.15),(74.33±6.34),(36.33±3.32),(20.67±2.26) and (13.67±0.89) cells;the relative protein expression levels of p-PI3K were 0.92±0.11,0.80±0.12,0.61±0.07,0.42±0.05 and 0.15±0.03;the relative protein expression levels of p-AKT were1.21±0.14,0.73±0.12,0.59±0.11,0.49±0.09 and 0.27±0.05.There were statistically significant differences in various experimental groups compared with those in control group (all P0.05),and the above indicators were dose-dependent in experimental groups (all P0.05).Conclusion TanshinoneⅡA can inhibit the growth,cloning,migration and invasion of OSCC cells,and promote the cell apoptosis,and it may play an anticancer role by inhibiting PI3K/AKT signaling pathway.
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