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将含有RA538的真核表达载体pCDV1与含neo基因的表达载体pDOR-neo经Lipofectin法共转染到人食管癌细胞系EC8712,EC109细胞,结果表明:RA538的表达对两细胞系均有很强的生长抑制作用,引起细胞形态的明显改变,诱发细胞终末分化与死亡。RT-PCR分析发现,RA538的表达激活了谷氨酰胺转移酶(transglutaminase,TGase)基因的表达,引起c-myc基因表达下降,被膜素(involu-crin)基因表达增加.而对TGF-β基因的表达没有明显的影响.应用凋亡细胞原位检测法证实,RA538表达诱发的细胞死亡是通过细胞凋亡而实现的.以上结果与直接用维甲酸处理人食管癌细胞后所得结果相似 因此认为:RA538是维甲酸诱导人食管癌细胞发生终末分化和凋亡过程中一系列被激活基因中的1个关键基因.
The eukaryotic expression vector pCDV1 containing RA538 and the expression vector pDOR-neo containing neo gene were co-transfected into human esophageal cancer cell line EC8712 and EC109 cells by Lipofectin method. The results showed that the expression of RA538 was strong for both cell lines. The growth inhibitory effect caused a significant change in cell morphology, inducing terminal cell differentiation and death. RT-PCR analysis showed that expression of RA538 activated transglutaminase (TGase) gene expression, resulting in decreased expression of c-myc gene and increased expression of involu-crin gene. There was no apparent effect on expression. Apoptotic cell in situ assays were used to confirm that cell death induced by RA538 expression was achieved by apoptosis. The above results are similar to those obtained after direct treatment of human esophageal cancer cells with retinoic acid. : RA538 is a key gene in a series of activated genes in the process of terminal differentiation and apoptosis of human esophageal cancer cells induced by retinoic acid.