青藤碱抑制人卵巢癌SKOV3细胞活力、迁移和侵袭

目的:观察青藤碱对人卵巢癌SKOV3细胞活力、迁移和侵袭的影响,并探讨其可能的分子机制。方法:分别采用不同浓度的青藤碱处理SKOV3细胞12、24和48 h,采用CCK-8法检测细胞活力,采用流式细胞术检测细胞周期,采用Transwell实验检测细胞迁移率和侵袭率,同时采用Western blot法检测细胞周期素(cyclin)A、cyclin D1、E-cadherin和基质金属蛋白酶9(matrix metalloproteinase-9,MMP-9)的蛋白表达水平。结果 :随着青藤碱作用浓度和作用时间的增加,SKOV3和IOSE80细胞活力逐渐降低,青藤碱作用SKOV3和IOSE80细胞48 h的半数抑制浓度(IC_(50))分别为2.12 mmol/L和17.35 mmol/L;青藤碱可呈剂量依赖性地诱导SKOV3细胞发生G_0/G_1期和S期阻滞(P0.05),抑制SKOV3细胞迁移和侵袭(P0.05),下调cyclin A、cyclin D1和MMP-9蛋白水平(P0.05),并上调E-cadherin蛋白水平(P0.05)。结论 :青藤碱可在体外抑制人卵巢癌SKOV3细胞活力、迁移和侵袭,这可能与其下调cyclin D1、cyclin A和MMP-9蛋白水平,以及上调E-cadherin蛋白水平有关。

Sinomenine inhibits viability,migration and invasion of human ovarian cancer SKOV3 cells

AIM:To investigate the effect of sinomenine on the viability, migration and invasion of human ovarian cancer SKOV3 cells and its possible mechanism. METHODS:The SKOV3 cells were treated with sinomenine at different concentrations for 12 h, 24 h and 48 h. CCK-8 assay was employed to detect the effects of sinomenine on the viability of the SKOV3 cells. Flow cytometry was used to analyze the cell cycle distribution. The cell migration and invasion abilities were measured by Transwell assay. Western blot was used to determine the protein levels of cyclin A, cyclin D1, E-cadherin and matrix metalloproteinase-9 (MMP-9). RESULTS:Sinomenine remarkably inhibited the viability of SKOV3 cells and IOSE80 cells in a time-dependent and dose-dependent manner (P<0.05), and the IC₅₀ values of 48 h were 2.12 mmol/L and 17.35 mmol/L, respectively. In a dose-dependent manner, sinomenine induced G₀/G₁ and S phase arrest in SKOV3 cells (P<0.05), suppressed the migration and invasion abilities of SKOV3 cells (P<0.05), down-regulated the protein levels of cyclin A, cyclin D1 and MMP-9 (P<0.05), and up-regulated the protein level of E-cadherin (P<0.05). CONCLUSION:Sinomenine inhibits the viability, migration and invasion of human ovarian cancer SKOV3 cells most likely via down-regulation of the protein levels of cyclin A, cyclin D1 and MMP-9, and up-regulation of the protein level of E-cadherin.