scRNA-sequencing raw data of LUAD
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Chemotherapy have been widely applied to the comprehensive treatment of lung adenocarcinoma (LUAD) patients, but its effect on immune microenvironment of lung adenocarcinoma needs further study. We obtained a total of 83622 cells derived from the tumor samples of nine LUAD patients who received only surgery or neoadjuvant chemotherapy. Functional enrichment analysis revealed that chemotherapy drove significant metabolic reprogramming in tumor cells and macrophages, which explained its enhanced malignancy and tumor-promoting phenotype after neoadjuvant treatment. Moreover, through analyzing the remodeling of T and B cells induced by neoadjuvant therapy, we noted that chemotherapy ignited a relatively stronger immune cytotoxic response towards tumor cells. Besides, a series of marker genes of different cell types and driver genes motivating phenotype shifting, such as metabolic reprogramming, were identified. Also, we constructed cell-to-cell crosstalk atlas based on tumor and immune cells at the single-cell level. In summary, our study demonstrates the metabolic reprogramming within the TME of LUAD induced by chemotherapy.
化疗已被广泛应用于肺腺癌(Lung Adenocarcinoma, LUAD)患者的综合治疗,但其对肺腺癌免疫微环境的影响仍有待进一步研究。本研究共收集9名仅接受手术或新辅助化疗的肺腺癌患者的肿瘤样本,共计获得83622个细胞。功能富集分析结果显示,化疗可诱导肿瘤细胞与巨噬细胞发生显著的代谢重编程,这解释了新辅助化疗后肿瘤细胞恶性程度升高、促肿瘤表型增强的现象。此外,通过分析新辅助治疗诱导的T细胞与B细胞重塑情况,本研究发现化疗可触发针对肿瘤细胞的更强免疫细胞毒性应答。本研究还鉴定出了多种细胞类型的标志性基因,以及驱动表型转变(如代谢重编程)的驱动基因。同时,基于单细胞层面的肿瘤细胞与免疫细胞数据,本研究构建了细胞间互作图谱。总结而言,本研究证实了化疗可诱导肺腺癌肿瘤微环境(Tumor Microenvironment, TME)内的代谢重编程。




