ROCK通路在DLC-工基因调控人结肠癌HT29细胞侵袭中的作用

目的 观察肝癌缺失基因1(DLC-1)对HT-29细胞侵袭能力的影响.方法 用脂质体法将重组质粒pcDNA3.1-DLC-1转染HT-29细胞;应用Rho激酶(ROCK)特异性抑制剂Y27632处理HT-29细胞;Western blot检测p-MLC蛋白表达;Transwell小室实验检测细胞侵袭能力.结果 野生型HT-29细胞DLC-1基因表达呈阴性,经转染获得DLC-1稳定表达细胞系;与对照组及空载组HT-29细胞相比,转染组和ROCK抑制剂组p-MLC蛋白表达均下调,细胞侵袭能力受到抑制(P<0.05).结论 转染DLC-1基因可能通过抑制ROCK活性,从而抑制HT-29细胞的侵袭能力.

Effects of DLC-1 gene transfection on HT29 cell invasion: the role of ROCK signal pathway

Objective To investigate the effects of frequently deleted in liver (DLC-1) gene transfection on HT29 cell invasioa Methods Recombinant pcDNA3.1 vector containing the DLC-1 gene was constructed and transfected into HT29 cell line. HT29 cell was treated with Rho-associated kinase(ROCK) inhibitor Y27632. The expression of p-MLC was examined by Western blotting. The invasion ability was detected by transwell. Results The HT-29 cells rarely expressed DLC-1 mRNA and the transfected HT-29 cells could express DLC-1 mRNA steadily. Significant down-regulation of p-MLC expression and decreased invasive ability of DLC-1 were seen in groups of transfected and ROCK inhibited HT29 cells. Conclusion Overexpression of DLC-1 gene caused significantly down-regulation of ROCK activity, which may further inhibit the invasiof HT29 cells.