Objective Loss-of-function mutation of p53,a tumor suppressor gene,is an important mechanism for the development of human cancers.In this study we tried to transfect p53N15-based fusion peptide into H1299,a lung cancer cell line,and evaluate the anti-tumor effects of the fusion peptide.Methods Adeno-associated virus ( AAV) vectors were used for transfecting p53N15 fusion peptide into p53-null lung adenocarcinoma H1299 cells.The anti-replication effects of p53N15 fusion peptide were evaluated with inverted microscopy,MTT test for cell viability and flow cytometry.Results Fusion peptides in H1299 cells was highly expressed and had detectable suppressive effects on cell proliferation.A large amount of dead cells were seen under microscope after the transfection of recombinant viruses for 72 hours.Cells activity was reduced significantly in the virus-transfecting groups as demonstrated by MTT test.The flow cytometry showed that a large number of dead cells were present in the virus-transfecting groups.Conclusion The growth of H1299 lung adenocarcinoma cells could be inhibited in vitro by being transfected with p53N15 fusion peptide,which may be a potential gene therapy alone or as an adjuvant option in the treatment of lung cancer.%目的 探讨p53N15融合肽转染对肺腺癌细胞H1299体外生长的抑制作用.方法 通过腺体相关病毒(adeno-associated virus AAV)载体把p53N15融合肽高效导入p53缺失肺腺癌H1299细胞系,应用相差倒置显微镜观察、MTT细胞活性试验及流式细胞仪技术分析p53N15对肺癌细胞的抑制作用.结果 p53N15融合肽在H1299细胞中得到了高效表达并发挥明显效应,表现为显微镜下,重组病毒转染72 h可见大片细胞死亡.MTT试验分析,重组病毒转染组细胞活性明显降低.流式细胞仪技术显示,重组病毒转染组可见大量死亡细胞.结论 p53N15融合肽转染可明显抑制肺腺癌细胞H1299的体外生长.
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