白细胞介素6促进人胰腺癌细胞的侵袭及机制探讨

摘要

目的 应用白细胞介素6(IL-6)作用于人胰腺癌细胞株SW1990和Capan-2,观察侵袭能力的变化并探讨其机制.方法 使用IL-6处理人胰腺癌细胞株SW1990和Capan-2,MTT法检测细胞增殖,免疫细胞化学和Western印迹检测P-STAT3的表达,荧光定量PCR、Western印迹检测VEGF、MMP-2 mRNA和蛋白表达,体外侵袭检测细胞的侵袭能力.结果 IL-6 100 μg/L作用人胰腺癌细胞株后,细胞增殖能力增强(P＜0.05);Western印迹和免疫细胞化学显示P-STAT3的表达增加;荧光定量PCR、Western印迹显示VEGF、MMP-2的mRNA和蛋白表达明显升高(P＜0.05);细胞侵袭能力增强.结论 IL-6通过激活STAT3信号转导通路,上调MMP-2和VEGF表达,增强胰腺癌细胞侵袭能力.%Objective To investigate the effects and mechanism of IL-6 on invasion and metastasis of human pancreatic cancer cells. Methods IL-6 was added into the culture media of human pancreatic cancer cells Capan-2 and SW1990. Cell growth was measured by MTT assay. Western blot and immunocytochemistry were performed to detect Phosphorylated STAT3 (P-STAT3) protein. VEGF and MMP-2 mRNA and protein expression were examined using fluorescence quantitative polymerase chain reaction (RT-PCR) and Western blot, respectively. The invasion ability of SW1990 and Capan2 cells was determined by cell invasion assay in vitro. Results 100 ng/mL IL-6 significantly promoted growth and invasion ability of Capan-2 and SW1990 cells (P＜0.05). The use of IL-6 not only markedly increased the protein expression of P-STAT3, VEGF and MMP-2, but also greatly increased the mRNA expression of MMP-2 and VEGF. Conclusions STAT3 signal transducer pathway activation with IL-6 can promote the invasion ability of pancreatic cancer cells in vitro through up-regulation of MMP-2 and VEGF expression. STAT3 signal transducer may provide a novel therapeutic target for the treatment of pancreatic cancer.