作为生物和医学领域的科学家，您精通英语和简体中文。将以下文章翻译成准确且符合学术论文语言模式的简体中文，保持原句结构： 肺腺癌（LUAD）作为最常见的肺癌类型，对公共卫生构成了重大威胁。肿瘤的异质性在癌症发生中起着关键作用，这可以通过下一代测序（NGS）来大致解读。我们获取并筛选了16个LUAD样本的单细胞RNA测序（scRNA-seq）数据，并将内皮细胞（ECs）分为三个类群。我们通过伪时序分析来探索EC分化的起源。我们使用CellChat分析来检测EC与恶性细胞之间的潜在通信，使用基因调控网络分析来确定转录因子活性的变化。我们在大量转录组水平上探究了特定EC类群的预后及其对肿瘤微环境（TME）的影响。我们进行了5-乙炔基-2'-脱氧尿嘧啶（EdU）和Ki-67染色，以研究LUAD细胞系的增殖表型。利用针对PI3K-AKT蛋白质磷酸化的Western blotting确定NCL的下游通路。COL3A1阳性的ECs表现出与恶性细胞最高的相互作用，表明它们对于驱动LUAD的癌变具有重要作用。我们确定了血管内皮生长因子（VEGF）信号通路作为主要信号通路，介导恶性细胞的信号转导。COL3A1阳性ECs的TME相关基因表达显著更高。COL3A1阳性ECs表现出独特的代谢和免疫特征，以及高度活化的代谢信号通路和炎症反应。重要的是，COL3A1阳性ECs分数低的LUAD患者显示出较差的预后结果和更高的转移风险。通过筛选，我们确定了介入上皮细胞和癌细胞间相互作用的关键靶基因NCL。流式细胞术显示NCL的减少促进了A549和NCI-H1299的凋亡。Western blotting显示NCL的减少降低了AKT和PI3K的磷酸化水平，从而确定了NCL的下游通路。COL3A1阳性ECs对LUAD的发展和免疫微环境的形成具有重要作用。此外，我们还确定了一个在内皮细胞和癌细胞间相互作用中发挥作用的关键靶基因NCL。NCL还通过PI3K-AKT信号通路影响LUAD的凋亡和增殖。© 2023 John Wiley & Sons Ltd.

Lung adenocarcinoma (LUAD), as the most common type of lung cancer, poses a significant threat to public health. Tumor heterogeneity plays a crucial role in carcinogenesis, which could be largely deciphered by next-generation sequencing (NGS).We obtained and screened single-cell RNA sequencing (scRNA-seq) data from 16 LUAD samples, and endothelial cells (ECs) were grouped into three clusters. The origin of EC differentiation was explored by pseudo-time analysis. CellChat analysis was used to detect potential communication between ECs and malignant cells, and gene regulatory network analysis was used to identify changes in transcription factor activity. We explored the prognosis of specific ECs clusters and their effects on the tumor microenvironment (TME) at the bulk transcriptome level. 5-Ethynyl-2'- deoxyuridine (EdU) and Ki-67 staining were conducted to study the proliferative phenotype of LUAD cell lines. Western blotting targeting the phosphorylation of PI3K-AKT proteins was utilized for determination of the downstream pathway of NCL.COL3A1-positive ECs showed the highest crosstalk interaction with malignant cells, indicating that they have important effects on driving LUAD carcinogenesis. Vascular endothelial growth factor (VEGF) signaling pathway was identified as the main signaling pathway, mediating signal transduction from malignant cells. The TME-related genes of COL3A1-positive ECs were significantly more highly expressed. COL3A1-positive ECs showed unique metabolic and immune characteristics, as well as highly activated metabolic signaling pathways and inflammatory responses. Importantly, LUAD patients with low COL3A1-positive ECs scores displayed an inferior prognosis outcome and a higher risk of metastasis. The key target gene NCL, which is involved in the interaction between epithelial cells and cancer cells, has been identified through screening. Flow cytometry showed that knockdown of NCL prompted the apoptosis of A549 and NCI-H1299. Western blotting showed that knockdown of NCL decreased the phosphorylation of AKT and PI3K, which identified the downstream pathway of NCL.COL3A1-positive ECs have important effects on the development of LUAD and the formation of an immune microenvironment. Furthermore, we identified a key target gene, NCL, which is involved in the interaction between endothelial cells and cancer cells. NCL also affected the apoptosis and proliferation in LUAD through the PI3K-AKT pathway.© 2023 John Wiley & Sons Ltd.