目的：研究siRNA干扰X连锁凋亡抑制蛋白（Xlinked inhibitor of apoptosis protein, XIAP）基因表达对结肠癌细胞LoVo体内外增殖的影响。方法：构建XIAP真核表达干扰载体pSil2.1shXIAP1和pSil2.1shXIAP2，脂质体转染结肠癌细胞株LoVo，G418筛选出稳定转染LoVoshXIAP2细胞。RTPCR和Western blotting方法检测XIAP mRNA和蛋白的表达。MTT法和平板克隆形成实验检测LoVo细胞的增殖；流式细胞仪检测细胞的凋亡；裸鼠移植瘤模型观察XIAP表达下调对结肠癌体内增殖活性的影响。结果：LoVoshXIAP2细胞中XIAP mRNA和蛋白表达水平均显著下调。相对于对照组细胞，LoVoshXIAP2细胞的增殖和克隆形成率显著降低(P<0.01），凋亡率显著增加（P<0.01）。 LoVoshXIAP2移植瘤组织中XIAP蛋白表达明显下调，LoVoshXIAP2移植瘤生长显著抑制（均P<0.05）。结论：pSil2.1shXIAP2能够抑制结肠癌LoVo细胞中XIAP蛋白的表达，抑制LoVo细胞体内外的增殖，有望成为结肠癌免疫治疗的新手段。

Objective:To investigate the effect of XIAP (Xlinked inhibitor of apoptosis protein)targeting siRNA on the proliferation of LoVo colorectal cancer cells in vitro and in vivo. Methods: The XIAPtargeting siRNA pSil2.1shXIAP1 and pSil2.1shXIAP2 eukaryotic vectors were constructed and were transfected into LoVo cells using Lipofectamine; the stable transfectants LoVoshXIAP2 were selected by G418. The expressions of XIAP mRNA and protein were determined by RTPCR and Western blotting. The proliferation of LoVo cells was determined by MTT and colony formation assay. Cell apoptosis was examined by FCM. The influence of XIAP knockdown on the proliferation of LoVo cells in vivo was observed in LoVobearing nude mice. Results:The expressions of XIAP mRNA and protein in LoVoshXIAP2 cells were significantly downregulated in LoVoshXIAP2 cells. Compared with untransfected LoVo cells, the proliferation and colony formation abilities of LoVoshXIAP2 cells were significantly inhibited (P<0.05); the apoptosis rate of LoVoshXIAP2 cells was significantly increased (P<0.05). The expression of XIAP protein in LoVoshXIAP2 implanted tumors was downregulated and the growth of tumors was significantly inhibited (all P<0.05). Conclusion: pSil2.1shXIAP2 plasmid can downregulate the expression of XIAP in LoVo cells and inhibit proliferation of LoVo cells in vitro and in vivo, making XIAPtargeting siRNA a potential new agent in immune therapy of colorectal cancer.