间隙连接基因Cx43表达对肺癌细胞体内成瘤生长的抑制

目的探讨间隙连接基因表达和细胞通讯功能对肿瘤生长的抑制作用。方法以高转移性人肺癌ＰＧ细胞为材料,该细胞的间隙连接基因Ｃｘ４３表达抑制,细胞通讯功能缺陷。用Ｃｘ４３ｃＤＮＡ转染ＰＧ细胞,分离转染子克隆,与只转染空载体ｃＤＮＡ的对照组ＰＧ进行比较。用Ｎｏｒｔｈｅｒｎ分子杂交和染料传输方法检查间隙连接表达情况,并观察细胞在体外和裸鼠体内生长。结果空载体对照组与未转染组ＰＧ相似,Ｃｘ４３ｍＲＮＡ无表达,通讯功能缺陷,细胞生长快,在软琼脂内集落形成率高（１１．６％）,植入裸鼠体内２８天,平均瘤重３．４７ｇ。转染组细胞Ｃｘ４３ｍＲＮＡ表达升高,通讯功能增强,细胞生长慢,在软琼脂内集落形成率和在裸鼠体内生长速度明显低于对照组,抑制率分别为９０％和７５％。结论间隙连接基因Ｃｘ４３表达对肺癌细胞有抑瘤作用。

Inhibition of in vivo growth of lung carcinoma cells after transfection with gap junction gene Cx43

Objective To explore the effects of expression of gap junction gene and cell cell communication on tumor growth. Methods A highly metastatic human lung carcinoma cell line PG was used. PG cells were defective of gap junctional intercellular communication(GJIC) and lacking expression of gap junction gene Cx43. By transfection, Cx43 cDNA was introduced into PG cells and blank vector cDNA was used as mock control. By using Northern blot, dye transfer methods and examinations of in vitro/in vivo growth,stable Cx43 transfectant cells were studied. Results The mock control cells resembled untransfected PG cells in lacking expression of Cx43 and GJIC function. They grew fast in soft agar(colony formation rate 11.6%) and in nude mice (average tumor weight 3.47 g in 28 days). The Cx43 transfectant cells showed increased level of Cx43 mRNA and increased function of GJIC. Cell growth in soft agar and in nude mice was markedly retarded. The inhibition rate was 90% and 75%, respectively. Conclusion Increased expression of gap junction gene Cx43 induced tumor suppressing effects in human lung carcinoma cells.