Objective： The aim of our study was to investigate the biological effects of Bcl-XL antisense oligodeoxynucleotide （ASODN） transfected into cultured esophageal carcinoma cells and human esophageal carcinoma xenogra...Objective： The aim of our study was to investigate the biological effects of Bcl-XL antisense oligodeoxynucleotide （ASODN） transfected into cultured esophageal carcinoma cells and human esophageal carcinoma xenograft in nude mice. Methods： Cationic liposome-mediated ASODN was used to transfect esophageal carcinoma cells. RT-PCR, Western blot, MTT assay, flow cytometry, and in situ apoptosis cells detection （TUNEL detection） were used to systematically study the biological effects of transfected cells both in vitro and in vivo. Results： In this study, the results showed that the proliferation of esophageal carcinoma cells in ASODN group decreased significantly when compared with the control group （P 〈 0.05）, at 57.3% Bcl-XL mRNA inhibitory rate, and a significant decreasing of Bcl-XL protein expression, at the apoptosis rates of （31.1 ＋ 5.8）% and 35.0% by flow cytometry and TUNEL assay respectively （P 〈 0.01, when compared with control groups）. It also showed that the growth of human esophageal carcinoma in nude mice of ASODN group was significantly inhibited （P 〈 0.05）, together with a significant decreased expression level of Bcl-XL mRNA and protein, and an induced tumor cell apoptosis in nude mice. Conclusion： Our result indicates BcI-XL ASODN can effectively inhibit the proliferation of esophageal carcinoma cells in vitro and tumor growth in vivo. The suppression of Bcl-XL expression by ASODN may offer both a therapeutic approach and an important theoretic foundation for gene therapy against esophageal carcinoma.展开更多
基金Supported by a grant from the Henan Innovation Project for University Prominent Research Talents (No. 2007KYCX005)
文摘Objective： The aim of our study was to investigate the biological effects of Bcl-XL antisense oligodeoxynucleotide （ASODN） transfected into cultured esophageal carcinoma cells and human esophageal carcinoma xenograft in nude mice. Methods： Cationic liposome-mediated ASODN was used to transfect esophageal carcinoma cells. RT-PCR, Western blot, MTT assay, flow cytometry, and in situ apoptosis cells detection （TUNEL detection） were used to systematically study the biological effects of transfected cells both in vitro and in vivo. Results： In this study, the results showed that the proliferation of esophageal carcinoma cells in ASODN group decreased significantly when compared with the control group （P 〈 0.05）, at 57.3% Bcl-XL mRNA inhibitory rate, and a significant decreasing of Bcl-XL protein expression, at the apoptosis rates of （31.1 ＋ 5.8）% and 35.0% by flow cytometry and TUNEL assay respectively （P 〈 0.01, when compared with control groups）. It also showed that the growth of human esophageal carcinoma in nude mice of ASODN group was significantly inhibited （P 〈 0.05）, together with a significant decreased expression level of Bcl-XL mRNA and protein, and an induced tumor cell apoptosis in nude mice. Conclusion： Our result indicates BcI-XL ASODN can effectively inhibit the proliferation of esophageal carcinoma cells in vitro and tumor growth in vivo. The suppression of Bcl-XL expression by ASODN may offer both a therapeutic approach and an important theoretic foundation for gene therapy against esophageal carcinoma.
