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阳性COL3A1内皮细胞影响LUAD预后,并通过NCL-PI3K-AKT轴调节LUAD致癌

Moyan Zhang¹, Yicheng Liang², Peng Song¹

¹Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

The journal of gene medicine

|August 7, 2023

概括

阳性COL3A1内皮细胞通过与恶性细胞相互作用驱动肺腺癌 (LUAD). 向NCL可以通过PI3K-AKT途径抑制LUAD的进展,为这种癌症提供新的治疗策略.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

肺腺癌 (LUAD) 是一个主要的公共卫生问题.
通过下一代测序 (NGS) 解读的瘤异质性在LUAD致癌过程中至关重要.

研究的目的:

研究内皮细胞 (ECs) 在LUAD发育和瘤微环境 (TME) 中的作用.
为了确定LUAD治疗的关键分子标.

主要方法:

16个LUAD样本的单细胞RNA测序 (scRNA-seq) 用于集群ECs.
细胞通讯和转录因子活动的CellChat和基因调控网络分析.
预后分析,EDU/Ki-67染色,以及用于途径分析的西部斑点.

主要成果:

COL3A1阳性ECs与恶性细胞呈现显著的交叉声,驱动LUAD.
在VEGF信号通路中介通信; COL3A1阳性ECs显示独特的代谢和免疫特征.
低的COL3A1阳性ECs得分与预后不佳和转移风险增加相关.
NCL被确定为一个关键的基因,通过PI3K-AKT通路影响细胞亡和增殖.

结论:

COL3A1阳性EC在LUAD发育和免疫微环境形成中至关重要.
NCL是EC癌细胞相互作用的关键媒介,并影响LUAD的进展.
NCL通过PI3K-AKT通路影响LUAD亡和扩散,这表明了治疗潜力.

关键词:

在 COL3A1A1 中.在NCL中,NCL是指NCL.生物信息学是一种生物信息学.内皮细胞是内皮细胞.肺部腺癌的癌症.

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