转化生长因子βⅠ型受体多态性在结肠癌细胞侵袭迁移中的作用

The function of TGF-β receptor type 1 gene* 6A on the invasion and migration of the colorectal carcinoma cells

目的探讨转化生长因子βⅠ型受体多态性——TGF-βRⅠ6A在结肠癌SW48和DLD-1细胞侵袭转移中的作用。方法将TGF-βRⅠ6A基因转染SW48和DLD-1细胞,MTT法检测TGF-βRⅠ6A对结肠癌细胞增殖能力的影响;MatrigelTM侵袭试剂盒检测转染TGF-βRⅠ6A后细胞侵袭迁移能力的变化。Western blot检测TGF-βRⅠ6A在TGF-β1作用下,SW48细胞中ERK、磷酸化ERK、p38、磷酸化p38、Smad2和磷酸化Smad2基因的变化。结果转染TGF-βRⅠ6A的SW48细胞和DLD-1细胞,在TGF-β1(5ng/ml)的作用下,其体外增殖、侵袭、迁移能力均增强。此外SW48细胞中磷酸化ERK、磷酸化p38表达增强,Smad2和磷酸化Smad表达无明显变化。结论 TGF-βRⅠ6A在TGF-β1的作用下,能够增强SW48和DLD-1细胞的体外增殖、侵袭、迁移能力,可能与非Smad信号通路交联增强ERK、p38等基因的表达,从而促进结肠癌细胞侵袭迁移的作用有关。

Objective To elucidate the effect of TGF-βreceptor type 1 gene*6A on the migration and invasion of the colorectal carcinoma SW48 and DLD-1 cells.Methods TGF-βR1*6A was introduced into SW48 and DLD-1 cells by lipofectactin-mediated DNA transfection.RT-PCR and Western blot were used to determine TGF-βR1* 6A expression.The effects of the TGF-β1 on the proliferation of SW48 cells and DLD-1 cells which were transfected by TGF-βR1* 6A was determined by MTT.The effects of the TGF-β1 on the invasion of the SW48 cells and DLD-1 cells which were transfected were determined by MatrigelTM invasive chambers.The transforming migrating chambers were used to determine the effects of the TGF-β1 on the migration of the SW48 cells and DLD-1 cells which were transfected.Western blot were used to determine the gene expression of the ERK(Phosph-ERK),p38(Phosph-p38)and Smad2(Phosph-Smad2)in SW48 cells.Results The proliferation,invasion and migration of the SW48 cells and DLD-1cells which were transfected by TGF-βR1*6A were enhanced in the presence of TGF-β1 whose concentration was 5 ng/ml,whereas this phenomenon was not observed in the groups without TGF-β1.The gene expressions of ERK(Phosph-ERK)and p38(Phosph-p38)in SW48 cells which were transfected by TGF-βR1* 6A were enhanced,however the gene expression of Smad2(Phosph-Smad2)did not change.Conclusions TGF-βRI*6A enhances the proliferation,invasion and migration of the SW48 cells and DLD-1 cells in the presence of TGF-β1,and may enhance the gene expressions of the ERK and p38 to mediate the cancer promoting to the colorectal carcinoma cells by TGF-β1.