川陈皮素抑制胃癌SGC-7901细胞侵袭能力的机制探讨

目的:观察川陈皮素（nobiletin，Nob）对胃癌SGC-7901细胞侵袭能力的影响，并探讨其可能的作用机制。方法:不同浓度的川陈皮素（0、30、60、120 mg/L）体外处理SGC-7901细胞。CCK8法检测细胞增殖能力；Transwell小室法检测细胞侵袭能力的改变；免疫印迹法检测细胞上皮间质转化（epithelial-mesenchymal transition,EMT)标志物（E-cadherin、Vimentin、Fibronectin）蛋白、MMP-9、STAT3、p-STAT3蛋白表达的改变。结果:CCK8和Transwell小室法检测结果显示，与对照组（0 mg/L）比较，川陈皮素可显著抑制SGC-7901细胞的增殖和侵袭能力；免疫印迹结果显示，随着川陈皮素浓度的增加，SGC-7901细胞E-cadherin蛋白表达逐渐上调，同时Vimentin、Fibronectin蛋白的表达量降低，MMP-9蛋白表达下调,STAT3总量未发生变化，但p-STAT3表达逐渐降低。结论:川陈皮素可降低胃癌SGC-7901细胞侵袭能力，其机制可能为通过抑制STAT3通路，继而抑制EMT。

Study on the mechanism of nobiletin inhibiting the invasiveness of SGC-7901 gastric cancer cells

Objective:To investigate the effect of nobiletin(Nob) on the cell invasiveness in SGC-7901 gastric cancer cells and explore the possible mechanisms.Methods:SGC-7901 cells were cultured in vitro.After treatment by nobiletin at different concentrations(0,30,60 and 120 mg/L) respectively,cell proliferation was detected by CCK8 assay and the invasion of SGC-7901 cells was tested by Transwell assay.Western blot was used for E-cadherin,Vimentin,Fibronectin,MMP-9,STAT3 and p-STAT3 protein analysis.Results:Results of CCK8 showed that cell proliferation was inhibited by nobiletin significantly and Transwell experiments revealed that the number of SGC-7901 cells treated by nobiletin passing through the basement membrane was less than that of the control group(P＜0.05),suggesting that nobiletin could inhibit the capacity of cell invasion.Nobiletin could promoted the expressions of E-cadherin,and suppressed the expressions of Vimentin,Fibronectin,MMP-9 and p-STAT3 in a dose-dependent manner.Conclusion:Nobiletin could inhibit the capacity of cell invasion,and the effects of antitumor may be associated with inhibition of the STAT3 signaling pathway,thus inhibiting of epithelial-to-mesenchymal transition in gastric cancer cell line SGC-7901 cells.