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首页> 外文期刊>Journal of Cellular Physiology >Cell-penetrating and endoplasmic reticulum-locating TAT-IL-24-KDEL fusion protein induces tumor apoptosis
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Cell-penetrating and endoplasmic reticulum-locating TAT-IL-24-KDEL fusion protein induces tumor apoptosis

机译：Cell-penetrating和内质的reticulum-locating TAT-IL-24-KDEL融合蛋白诱导肿瘤细胞凋亡

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摘要

Interleukin-24 (IL-24) is a unique IL-10 family cytokine that could selectively induce apoptosis in cancer cells without harming normal cells. Previous research demonstrated that intracellular IL-24 protein induces an endoplasmic reticulum (ER) stress response only in cancer cells, culminating in apoptosis. In this study, we developed a novel recombinant fusion protein to penetrate into cancer cells and locate on ER. It is composed of three distinct functional domains, IL-24, and the targeting domain of transactivator of transcription (TAT) and an ER retention four-peptide sequence KDEL (Lys-Asp-Glu-Leu) that link at its NH2 and COOH terminal, respectively. The in vitro results indicated that TAT-IL-24-KDEL inhibited growth in bladder cancer cells, as well as in non-small cell lung cancer cell line and breast cancer cell line, but the normal human lung fibroblast cell line was not affected, indicating the cancer specificity of TAT-IL-24-KDEL. Western blot analysis showed that apoptosis activation was induced by TAT-IL-24-KDEL through the ER stress-mediated cell death pathway. Treatment with TAT-IL-24-KDEL significantly inhibited the growth of human H460 xenografts in nude mice, and the tumor growth inhibition was correlated with increased hematoxylin and eosin (H&E) staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. These findings suggest that the artificially designed recombinant fusion protein TAT-IL-24-KDEL may be highly effective in cancer therapy and worthy of further evaluation and development. J. Cell. Physiol. 230: 84-93, 2016. (c) 2015 Wiley Periodicals, Inc.
机译：Interleukin-24 (IL-24)是一个独特的il - 10的家庭细胞因子,可以选择性地诱导细胞凋亡在肿瘤细胞而不损伤正常细胞。先前的研究表明,细胞内IL-24蛋白诱发内质网(ER)只在癌症细胞应激反应,在细胞凋亡。开发了一种新型重组融合蛋白进入癌症细胞ER和定位。由三个不同的功能领域,IL-24,反式激活因子的目标域的转录(乙)和一个ER保留four-peptide序列KDEL (Lys-Asp-Glu-Leu)分别连接在其氨基和羧基末端。体外结果表明TAT-IL-24-KDEL抑制膀胱癌的增长细胞,以及在非小细胞肺癌细胞系和乳腺癌细胞系,但不正常的人类肺成纤维细胞系影响,表明癌症特异性的TAT-IL-24-KDEL。激活细胞凋亡引起的通过ER stress-mediated TAT-IL-24-KDEL细胞死亡途径。显著抑制人类H460的增长在裸鼠异种移植肿瘤的生长抑制作用与增加苏木精和伊红染色和终端())原位dUTP尼克末端标记(TUNEL)染色。表明,人为地设计重组融合蛋白TAT-IL-24-KDEL高度有效的癌症治疗和有价值的进一步评估和发展。杂志。230:84 - 93年,2016年。期刊、公司。

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