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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

神经元素通过激活NF-κB信号通路促进非小细胞肺癌的进展

卷 24, 期 11, 2024

发表于: 30 January, 2024

页: [1128 - 1143] 页: 16

弟呕挨: 10.2174/0115680096271746240103063325

价格: $65

摘要

背景与目的:了解神经蛋白(NNAT)在非小细胞肺癌(NSCLC)中的调控机制是一个持续的挑战。本研究旨在通过体外和体内两种方法阐明NNAT敲低对NSCLC的影响。 方法:为了研究NNAT的作用,我们在NSCLC细胞系A549和H226中沉默NNAT的表达。随后,评估各种参数,包括细胞增殖、侵袭、迁移和凋亡。此外,我们还建立了细胞来源的异种移植模型来评估NNAT敲除对肿瘤生长的影响。在体外和体内检测细胞周期蛋白D1、b细胞白血病/淋巴瘤2 (Bcl-2)、p65、基质金属蛋白酶(MMP) 2、神经生长因子(NGF)等关键分子的表达。用银染色法分析肿瘤组织内神经纤维密度。 结果:NNAT敲除后,观察到NSCLC细胞增殖、侵袭和迁移显著减少,同时细胞凋亡水平升高。此外,cyclin D1、Bcl-2、MMP2和磷酸化p65 (p-p65)的表达显著下调。在体内,NNAT敲低导致肿瘤生长明显抑制,同时肿瘤组织中cyclinD1、Bcl-2、MMP2和p-p65表达降低。重要的是,NNAT敲低还导致异种移植肿瘤组织中神经纤维密度下降和NGF表达下调。 结论:总的来说,这些发现表明神经元蛋白在推动NSCLC进展中起着关键作用,可能是通过激活核因子- κ B信号级联。此外,神经蛋白可能参与调节非小细胞肺癌的肿瘤微环境神经支配。靶向神经蛋白抑制是一种很有前途的抗非小细胞肺癌治疗干预策略。

关键词: 非小细胞肺癌,神经蛋白,核因子κ B,异种移植模型,体外,体内。

图形摘要
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