目的 探讨Bcl-xL基因对大肠癌细胞侵袭的影响及可能机制。方法 应用Bcl-xL基因小干扰RNA（small interfering RNA，siRNA）转染处理人大肠癌HT29细胞后，分别采用荧光实时定量RT-PCR和Western blot检测Bcl-xI基因mRNA和蛋白水平，分别采用软琼脂集落培养试验和Boydcn小室模型试验检测癌细胞的锚着不依赖性增殖和侵袭能力。另外，采用Western blot方法检测癌细胞尿激酶纤溶酶原激活物（urokinase-type plasminogen activator，uPA）蛋白变化。结果 转染组癌细胞Bcl-xL基因mRNA和蛋白水平明显被抑制，且与时间和浓度相关。与对照组比较，转染组细胞所形成的软琼脂集落数和穿膜细胞数明显减少，且呈浓度依赖性门转染组癌细胞uPA蛋白水平明显下降，且与浓度相关。结论Bcl-xL基因在大肠癌细胞侵袭中起着重要的作用；以siRNA下调Bcl-xL基因表达，可明显抑制大肠癌细胞恶性侵袭，其机制可能与下调uPA表达有关。

Objective To study the effects and mechanism of Bcl-xL, gene on invasion of human colon cancer cell. Methods After human colon cancer cell line HT29 was transfected by Bcl-xL, small interfering RNA (siRNA), the mRNA and protein of Bcl-xL were determined by real time RT-PCR and Western blot assay respectively. The anchorage-independent growth was examined by clones formation in soft agar, and invasion ability was evaluated by hoyden chamber model. Besides, the protein level of urokinase-type plasminogen activator (uPA) was also determined by Western blot assay. Results Bcl-xL siRNA could inhibit anchorage-independent growth and invasion ability in dose-dependent patters, respectively. Meanwhile，Bcl-xL siRNl1 reduced uPA protein level in colon cancer cell. Conclusions RNA interference Bcl-xL gene can inhibit the invasion of colon cancer through down-regulating uPA expression.