首页> 外文期刊>Journal of microbiology and biotechnology >Potentiation of Apoptin-Induced Apoptosis by Cecropin B-Like Antibacterial Peptide ABPs1 in Human HeLa Cervical Cancer Cell Lines is Associated with Membrane Pore Formation and Caspase-3 Activation
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Potentiation of Apoptin-Induced Apoptosis by Cecropin B-Like Antibacterial Peptide ABPs1 in Human HeLa Cervical Cancer Cell Lines is Associated with Membrane Pore Formation and Caspase-3 Activation

机译:Cecropin B样抗菌肽ABPs1在人HeLa宫颈癌细胞系中由Apoptin诱导的细胞凋亡增强与膜孔形成和Caspase-3活化有关。

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Apoptin, a chicken anemia virus-encoded protein, induces apoptosis in chicken or human tumor cells, localizing in their nuclei as opposed to the cytoplasm of non-transformed cells. The present study was undertaken to investigate whether ABPs1 could potentiate apoptininduced apoptosis in HeLa cells. ABPs1 and the apoptin genes were successfully cloned into pIRES2-EGFP expression vector and expressed in HeLa cells. We report that ABPs1 augments apoptin cell growth inhibition in a concentration- and time-dependent manner. The DAPI staining and scanning electron microscopy observations revealed apoptotic bodies and plasma membrane pores, which were attributed to apoptin and ABPs1, respectively. Further, ABPs1 in combination with apoptin was found to increase the expression of Bax and to decrease the expression of survivin compared with either agent alone or the control. The apoptotic rate of HeLa cells treated with ABPs1 and apoptin in combination for 48 h was 53.95%. The two-gene combination increased the caspase-3 activity of HeLa cells. Taken together, our study suggests that ABPs1 combined with apoptin significantly inhibits HeLa cell proliferation, and induces cell apoptosis through membrane defects, up-regulation of Bax expression, down-regulation of survivin expression, and activation of the caspase-3 pathway. Thus, the combination of ABPs1 and apoptin could serve as a means to develop novel gene therapeutic agents against human cervical cancer.
机译:鸡贫血病毒编码蛋白Apoptin诱导鸡或人肿瘤细胞凋亡,定位于细胞核中,而不是未转化细胞的细胞质中。进行本研究以调查ABPs1是否能增强凋亡蛋白诱导的HeLa细胞凋亡。将ABPs1和凋亡蛋白基因成功克隆到pIRES2-EGFP表达载体中,并在HeLa细胞中表达。我们报告说,ABPs1以浓度和时间依赖的方式增加了对凋亡素细胞生长的抑制作用。 DAPI染色和扫描电镜观察发现凋亡小体和质膜孔,分别归因于凋亡小素和ABPs1。此外,发现与单独的药剂或对照相比,ABPs1与细胞凋亡蛋白的结合增加了Bax的表达并降低了survivin的表达。联合ABPs1和细胞凋亡素处理48 h的HeLa细胞凋亡率为53.95%。两种基因的组合增加了HeLa细胞的caspase-3活性。综上所述,我们的研究表明,ABPs1与细胞凋亡素联合可显着抑制HeLa细胞增殖,并通过膜缺损,Bax表达上调,survivin表达下调和caspase-3途径激活来诱导细胞凋亡。因此,ABPs1和细胞凋亡蛋白的组合可以作为开发针对人类宫颈癌的新型基因治疗剂的手段。

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