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当代肿瘤药物靶点

Editor-in-Chief

ISSN (Print): 1568-0096
ISSN (Online): 1873-5576

Research Article

CCKBR 表达下调抑制胃癌细胞增殖,揭示免疫毒素治疗的潜在靶点

卷 22, 期 3, 2022

发表于: 17 March, 2022

页: [257 - 268] 页: 12

弟呕挨: 10.2174/1568009622666220106113616

价格: $65

摘要

背景:据报道,在许多肿瘤中 CCKBR 表达密度或频率增加。 目的:我们旨在研究 CCKBR 是否促进胃癌 (GC) 的生长及其作为免疫毒素治疗靶点的潜力。 方法:使用慢病毒干扰系统产生CCKBR敲低的胃癌细胞。 Cell Counting Kit-8 和克隆形成测定用于评估细胞增殖。进行伤口愈合和细胞侵袭测定以评估细胞流动性。通过流式细胞术分析细胞周期。使用裸鼠异源肿瘤移植模型研究体内肿瘤生长。此外,我们生成了免疫毒素 FQ17P,并在体外评估了 FQ17P 的结合能力和肿瘤细胞毒性。 结果:CCKBR 表达的稳定下调导致 BGC-823 和 SGC-7901 细胞的增殖、迁移和侵袭减少。通过CCKBR过表达研究进一步验证了CCKBR对胃癌细胞的影响。 CCKBR 表达的下调也抑制了体内胃肿瘤的生长。此外,FQ17P 通过特异性结合肿瘤细胞表面的 CCKBR 杀死过表达 CCKBR 的 GC 细胞。 结论:CCKBR 蛋白驱动胃癌细胞的生长、迁移和侵袭,基于其异常表达、与胃泌素的功能结合相互作用以及随后的内化,它可能成为免疫毒素治疗的有希望的靶点。

关键词: CCKBR,核糖核酸干扰,胃癌增殖,靶向治疗,免疫毒素,FQ17P。

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