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本文根据有些肿瘤细胞表面富含δ型阿片受体的事实,化学合成了脑啡肽(Enk)N端5肽编码区,将其通过一连接3肽编码区与人α1型干扰素(IFN)基因相连,并在大肠杆菌中表达了这一融合蛋白。以体外培养的人结肠腺癌细胞和多形胶质瘤细胞为模型,采用~3H_1胸腺嘧啶核苷掺入法证明该融合蛋白抑制肿瘤细胞生长的活性显著高于单纯的IFN分子。通过Naloxone竞争阻断试验证明,这种抑制活性的增高确由Enk导向区介导。本文报道为IFN作用机制的研究提出了新课题,同时也展示了导向IFN治疗肿瘤的应用前景。
Based on the fact that some tumor cell surfaces are rich in δ-type opioid receptors, the enkephalin (Enk) N-terminal 5-peptide coding region was chemically synthesized and passed through a linking 3-peptide coding region and human α1 interferon (IFN). The genes were linked and this fusion protein was expressed in E. coli. Using human colonic adenocarcinoma cells and glioblastoma cells cultured in vitro as a model, ~3H_1 thymidine incorporation was used to demonstrate that the fusion protein inhibited the growth of tumor cells significantly higher than that of IFN alone. The Naloxone competitive blocking assay demonstrated that this increase in inhibitory activity is indeed mediated by the Enk guide region. This article presents a new topic for the study of the mechanism of IFN action, and also shows the application of IFN-oriented treatment of tumors.