摘要
AIM： To investigate whether the recombinant adenovirus induces the TNF-α-mediated apoptosis in vivo. METHODS： Human hepatocarcinoma cell line （HepG2） cells were transfected into BALB/c nude mice, and the tumor growth curve was drawn. We analyzed apoptosis in HepG2 cells by TUNEL, HE staining and electron microscopy. RESULTS： AdIκBαM was expressed stably and efficiently in HepG2 and could not be degraded by induction of TNF-α. Tumor growth in mice could be reduced remarkably if treated by AdIκBαM plus TNF-α. There was apoptosis of 〉 70% of cells treated with AdIκBαM plus TNF-α and about 50% of cells treated with AdIκBαM. In contrast, there was few cell apoptosis in HepG2 cells treated with phosphate buffered saline and AdIκBαM. HepG2 cells in mice also exhibited a high level of apoptosis after in vivo injection with AdIκBαM. The tumor growth curve indicated the tumor transfected with AdIκBαM could be restrained. CONCLUSION： AdIκBαM gene therapy greatly enhances apoptosis due to inhibition of an NF-κB-mediated antiapoptosis signaling pathway.
AIM: To investigate whether the recombinant adenovirus induces the TNF-α-mediated apoptosis in vivo.METHODS: Human hepatocarcinoma cell line (HepG2) cells were transfected into BALB/c nude mice, and the tumor growth curve was drawn. We analyzed apoptosis in HepG2 cells by TUNEL, HE staining and electron microscopy.RESULTS: AdIκBαM was expressed stably and eff iciently in HepG2 and could not be degraded by induction of TNF-α. Tumor growth in mice could be reduced remarkably if treated by AdIκBαM plus TNF-α. There was apoptosis of > 70% of cells treated with AdIκBαM plus TNF-α and about 50% of cells treated with AdIκBαM. In contrast, there was few cell apoptosis in HepG2 cells treated with phosphate buffered saline and AdIκBα. HepG2 cells in mice also exhibited a high level of apoptosis after in vivo injection with AdIκBαM. The tumor growth curve indicated the tumor transfected with AdIκBαM could be restrained.CONCLUSION: AdIκBαM gene therapy greatly enhances apoptosis due to inhibition of an NF-κB-mediated antiapoptosis signaling pathway.
基金
Supported by the Foundation of Hi-tech Research and Develop-ment Program of China (863 Program), No. 2001AA217121Co-fi rst-author: Li-Ping Jia
作者简介
Co-first-author： Li-Ping JiaCorrespondence to： Ling Gao, Center of Blood Purification, The 9th Hospital of Chongqing, Beibei 400700, Chongqing, China. gaoxiaochongqingm@sina.com Telephone： ＋86-23-68217675 Fax： ＋86-23-68862495
