中文摘要：

目的探讨下调CXCR4基因对甲状腺癌细胞SW579体外增殖和侵袭能力的影响及可能的机制。方法用脂质体2000将CXCR4-siRNA瞬时转染SW579细胞（RNAi组）,同时设立阴参组（只用脂质体而不用siRNA）和空白组（细胞不做任何处理）。通过MTT增殖实验和侵袭实验研究CXCR4对细胞增殖和侵袭能力的影响;采用Westernblot方法检测RNA干扰后ERK和AKT的磷酸化水平。结果 CXCR4表达水平下调后SW579细胞体外增殖能力减弱,增殖抑制率为32.2%。RNAi组侵袭的细胞数为13.8±1.48个,与空白组和阴参组比较显著减少（P〈0.01）。Western-blot结果显示RNA干扰后总AKT和磷酸化AKT水平均下降,以磷酸化AKT下降最为显著,而ERK表达水平无明显变化。结论通过RNA干扰下调CXCR4的表达能够显著抑制SW579细胞的增殖和侵袭能力;CXCR4对SW579细胞增殖和侵袭的影响可能是通过调节PI3K/AKT信号通路实现的。

英文摘要：

Objective To investigate the effect of CXCR4 down-regulation by RNA interference（ RNAi） on biological behavior of thyroid cancer cell SW579 in vitro and its possible mechanism. Methods CXCR4 specific siRNA was transiently transfected into SW579 cells by LipofectamineTM 2000（ RNAi group） . The cells were treated by lipofectamine only without siRNA in negative control group and cells were untreated in blank control group. The effect of CXCR4-siRNA on SW579 cell was observed by MTT proliferation assay and invasion assay. Western blot was used to detect the phosphorylation of ERK and AKT after RNA interference. Results After downregulation of CXCR4,the proliferation inhibition rate of SW579 cell was 32. 2% ,and the invasion cell number was 13. 8 ± 1. 48 respectively. They were significantly different from those of index in blank and negative controls（ P 0. 01） . Western blot results showed that total AKT and phosphorylated AKT significantly reduced in SW579 cells after RNA interference. Conclusion CXCR4 may regulate the biological behavior of SW579 cell through PI3K/AKT signal pathway. Down-regulation of CXCR4 by siRNA may affect the proliferation and invasion capacity of malignant thyroid cell by PI3K/AKT transduction pathway.