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目的:探讨丹参酮ⅡA对人胃癌细胞株MKN45体外侵袭转移能力的影响及其作用机制。方法:MKN45细胞体外培养,MTT法检测细胞增殖抑制率,细胞黏附侵袭实验检测细胞侵袭能力的改变,western blot检测各组培养细胞E-cadherin、CD44V6蛋白表达的变化。结果:与对照组比较,丹参酮ⅡA呈时间剂量性抑制胃癌MKN45细胞的增殖;各浓度丹参酮ⅡA处理组MKN45细胞与Matrigel胶的异质性黏附和侵袭、趋化能力均明显受抑制,有明显的剂量依赖性。western blot显示,丹参酮ⅡA能显著降低CD44V6蛋白、并上调E-cadherin蛋白的表达,与对照组相比,两者均剂量效应性显著。而不同时间组比较,E-cadherin蛋白按72h<48h略呈负相关趋势(P<0.05),CD44V6蛋白的时间梯度差异性不很明显(P>0.05)。结论:丹参酮ⅡA能抑制胃癌MKN45细胞侵袭和转移,其机制可能与直接抑制细胞侵袭转移活动,抑制MKN-45细胞相关基因蛋白CD44V6,促进黏附分子E-cadherin蛋白表达有关。
Objective: To investigate the effect of tanshinone ⅡA on invasion and metastasis of human gastric cancer cell line MKN45 and its mechanism. Methods: MKN45 cells were cultured in vitro. The inhibition rate of cell proliferation was detected by MTT assay. The invasion ability of cells was detected by cell adhesion and invasion assay. The expressions of E-cadherin and CD44V6 in cultured cells were detected by western blot. Results: Compared with the control group, tanshinone ⅡA inhibited the proliferation of gastric cancer MKN45 cells in a time-dose manner. Heterologous adhesion, invasion and chemotactic ability of MKN45 cells treated with tanshinone ⅡA at various concentrations were significantly inhibited Dose-dependent. Western blot showed that tanshinone Ⅱ A can significantly decrease CD44V6 protein and up-regulate the expression of E-cadherin protein, both of which have significant dose-response effects compared with the control group. Compared with different time groups, E-cadherin protein showed a slightly negative correlation at 72h <48h (P <0.05), and the difference in time gradient of CD44V6 protein was not significant (P> 0.05). CONCLUSION: Tanshinone IIA can inhibit the invasion and metastasis of gastric cancer MKN45 cells. The mechanism may be related to the direct inhibition of cell invasion and metastasis, the suppression of CD44V6 protein and the promotion of E-cadherin expression.