细胞骨架的重组和细胞粘附分子含量的变化在肿瘤细胞的转移扩散过程中至关重要。结直肠癌 (CRC) 细胞高表达 SMAD7，这是一种参与控制 CRC 细胞生长的蛋白质。在本研究中，我们评估了 SMAD7 是否调节 CRC 中的细胞骨架重组和动力学。在两种人类 CRC 细胞系 HCT116 和 DLD1 中，用特定反义寡核苷酸 (AS) 敲除 SMAD7，可降低迁移率和 F-ACTIN 丝的含量。 SMAD7 AS 处理细胞的基因阵列、实时 PCR 和蛋白质印迹显示 X 连锁凋亡抑制剂蛋白 (XIAP) 显着下调，XIAP 是凋亡抑制剂家族的成员，与该蛋白有关。在癌细胞迁移中。 IL-6 和 IL-22 这两种激活 STAT3 的细胞因子可增强癌细胞中的 XIAP，而这种诱导作用在 SMAD7 缺陷细胞中减弱。最后，在人类 CRC 中，SMAD7 mRNA 与 XIAP 表达相关。我们的数据表明，SMAD7 正向调节 CRC 细胞的 XIAP 表达和迁移，并提出了 SMAD7 控制 CRC 细胞骨架结构成分的机制。

The reorganization of the cell cytoskeleton and changes in the content of cell adhesion molecules are crucial during the metastatic spread of tumor cells. Colorectal cancer (CRC) cells express high SMAD7, a protein involved in the control of CRC cell growth. In the present study, we evaluated whether SMAD7 regulates the cytoskeleton reorganization and dynamics in CRC. Knockdown of SMAD7 with a specific antisense oligonucleotide (AS) in HCT116 and DLD1, two human CRC cell lines, reduced the migration rate and the content of F-ACTIN filaments. A gene array, real-time PCR, and Western blotting of SMAD7 AS-treated cells showed a marked down-regulation of the X-linked inhibitor of apoptosis protein (XIAP), a member of the inhibitor of apoptosis family, which has been implicated in cancer cell migration. IL-6 and IL-22, two cytokines that activate STAT3, enhanced XIAP in cancer cells, and such induction was attenuated in SMAD7-deficient cells. Finally, in human CRC, SMAD7 mRNA correlated with XIAP expression. Our data show that SMAD7 positively regulates XIAP expression and migration of CRC cells, and suggest a mechanism by which SMAD7 controls the architecture components of the CRC cell cytoskeleton.