Lin Z, Zhang Z, Wang N
Department of Cell Biology, Beijing Institute for Cancer Research, Beijing Medical University.
Zhonghua Zhong Liu Za Zhi. 1997 Jul;19(4):253-5.
To explore the effects of expression of gap junction gene and cell-cell communication on tumor growth.
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.
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.
Increased expression of gap junction gene Cx43 induced tumor-suppressing effects in human lung carcinoma cells.
探讨缝隙连接基因表达及细胞间通讯对肿瘤生长的影响。
采用高转移性人肺癌细胞系PG。PG细胞存在缝隙连接细胞间通讯(GJIC)缺陷,且缺乏缝隙连接基因Cx43的表达。通过转染,将Cx43 cDNA导入PG细胞,并以空白载体cDNA作为 mock对照。利用Northern印迹法、染料转移法以及体外/体内生长检测,对稳定的Cx43转染细胞进行研究。
mock对照细胞与未转染的PG细胞相似,缺乏Cx43表达和GJIC功能。它们在软琼脂中生长迅速(集落形成率为11.6%),在裸鼠体内生长也很快(28天时平均肿瘤重量为3.47 g)。Cx43转染细胞显示Cx43 mRNA水平升高,GJIC功能增强。在软琼脂和裸鼠体内的细胞生长明显受到抑制。抑制率分别为90%和75%。
缝隙连接基因Cx43表达增加可诱导人肺癌细胞产生肿瘤抑制作用。