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目的探讨丝裂原活化蛋白激酶(MAPK)磷酸酶1(MKP-1)在介导胰腺癌耐药细胞株SW 1990/Fu产生获得性耐药过程中的可能机制。方法采用Northern印迹杂交和W estern蛋白免疫印迹杂交方法,检测MKP-1在体外诱导建立的人胰腺癌耐药细胞株SW 1990/Fu、亲本细胞株SW 1990和胰腺癌细胞株M iaPaCa-2中的表达,分析MKP-1在SW 1990/Fu产生获得性耐药前后的变化。结果Northern印迹杂交结果显示,在SW 1990/Fu、SW 1990和M iaPaCa-2细胞株中均检测到2400 bp的MKP-1 mRNA,MKP-1在SW 1990/Fu的表达水平明显低于SW 1990和M iaPaCa-2。在蛋白水平上,W estern蛋白免疫印迹杂交结果也表明,与SW 1990和M iaPaCa-2相比,MKP-1蛋白在SW 1990/Fu细胞中的表达水平明显降低。结论MAPK家族的关键调节酶MKP-1可能参与SW 1990/Fu获得性耐药的产生,推测细胞信号转导系统的改变可能是导致胰腺癌细胞产生获得性耐药的机制之一。
Objective To investigate the possible mechanism of MAPK phosphatase 1 (MKP-1) -mediated resistance to pancreatic cancer cell line SW 1990 / Fu. Methods The human pancreatic cancer cell line SW 1990 / Fu induced by MKP-1 in vitro, the SW 1990 cell line and the pancreatic cancer cell line M iaPaCa-2 were detected by Northern blotting and Western blotting. The changes of MKP-1 before and after acquired acquired resistance of SW 1990 / Fu were analyzed. Results The result of Northern blot showed that 2,400 bp MKP-1 mRNA was detected in SW 1990 / Fu, SW 1990 and M iaPaCa-2 cell lines. The expression level of MKP-1 in SW 1990 / Fu was significantly lower than that in SW 1990 And M iaPaCa-2. At the protein level, Western blot analysis also showed that the expression level of MKP-1 protein was significantly decreased in SW 1990 / Fu cells compared to SW 1990 and MiaPaCa-2. Conclusion MKP-1, a key MAPK family regulator, may be involved in acquired drug resistance in SW 1990 / Fu. It is speculated that the alteration of cell signal transduction system may be one of the mechanisms leading to acquired drug resistance in pancreatic cancer cells.