姜黄素通过抑制Ras-ERK和Shh-GLI1信号诱导胰腺癌细胞凋亡  

Curcumin induces apoptosis of pancreatic cancer cells by inhibiting Ras-ERK and Shh-GLI1 signal pathways

作　　者：孙晓东[1] 刘杏娥[2] 

机构地区：[1]浙江大学医学院附属邵逸夫医院普外科,浙江杭州310016 [2]浙江医院肿瘤科,浙江杭州310013

出　　处：《中国病理生理杂志》2012年第6期996-1000,共5页Chinese Journal of Pathophysiology

基　　金：浙江省自然科学基金资助项目(No.Y2100434)

摘　　要：目的:探讨姜黄素对胰腺癌PANC-1细胞的影响及可能机制。方法:不同浓度的姜黄素作用于PANC-1细胞后,采用MTT法检测细胞增殖,流式细胞术检测细胞凋亡,Western blotting检测K-Ras、细胞外信号调节激酶1/2(ERK1/2)、磷酸化细胞外信号调节激酶(p-ERK1/2)、Sonic hedgehog(Shh)和胶质瘤相关癌基因同系物1(GLI1)的表达水平。结果:不同浓度的姜黄素与PANC-1细胞共培养后,浓度为30 mmol/L的姜黄素组能明显抑制PANC-1细胞的增殖,与其余各组相比,差异显著(P<0.01)。PANC-1细胞经30 mmol/L姜黄素处理后,其细胞凋亡率(37.57%)明显高于对照组(4.62%)(P<0.01)。经姜黄素处理的PANC-1细胞,其K-Ras、p-ERK、Shh和GLI1表达明显低于对照组(均P<0.01)。结论:姜黄素通过抑制Ras-ERK和Shh-GLI1信号通路的活化,抑制胰腺癌PANC-1细胞增殖,并诱导细胞凋亡。AIM： To investigate the effects of curcumin on pancreatic cancer cells and the possible molecular mechanisms. METHODS： The pancreatic cancer PANC-1 cells were treated with curcumin. Growth inhibitory rate of the cells was measured by MTT assay. Apoptosis of the cells was detected by flow cytometry. The expression levels of K-Ras,extracellular signal-regulated kinase 1/2（ERK1/2）,phosphorylated ERK1/2（p-ERK1/2）,Sonic hedgehog （Shh） and glioma-associated oncogene homolog 1（GLI1） were determined by Western blotting. RESULTS： The growth inhibitory rate of the cells in 30 mmol/L curcumin group was significantly different from that in other groups. Apoptotic rate in 30 mmol/L curcumin group （37.57%） was significantly higher than that in control group （4.62%）. The expression levels of K-Ras, p-ERK1/2, Shh and GLI1 in curcumin groups were significantly lower than those in control group. CONCLUSION： Curcumin inhibits proliferation and induces apoptosis of pancreatic cancer cells by inhibiting Ras-ERK and Shh-GLI1 signal pathways.

关 键 词：姜黄素 胰腺肿瘤 HEDGEHOG Ras-ERK通路 Shh-GLI1通路 

分 类 号：R735.9[医药卫生—肿瘤]