Huang Yiwei, Wu Gujie, Bi Guoshu, Cheng Lin, Liang Jiaqi, Li Ming, Zhang Huan, Shan Guangyao, Hu Zhengyang, Chen Zhencong, Lin Zongwu, Jiang Wei, Wang Qun, Xi Junjie, Yin Shanye, Zhan Cheng
Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Department of Pathology, Albert Einstein College of Medicine, Bronx, United States.
Elife. 2024 Dec 27;13:RP95988. doi: 10.7554/eLife.95988.
Chemotherapy is widely used to treat lung adenocarcinoma (LUAD) patients comprehensively. Considering the limitations of chemotherapy due to drug resistance and other issues, it is crucial to explore the impact of chemotherapy and immunotherapy on these aspects. In this study, tumor samples from nine LUAD patients, of which four only received surgery and five received neoadjuvant chemotherapy, were subjected to scRNA-seq analysis. In vitro and in vivo assays, including flow cytometry, immunofluorescence, Seahorse assay, and tumor xenograft models, were carried out to validate our findings. A total of 83,622 cells were enrolled for subsequent analyses. The composition of cell types exhibited high heterogeneity across different groups. Functional enrichment analysis revealed that chemotherapy drove significant metabolic reprogramming in tumor cells and macrophages. We identified two subtypes of macrophages: Anti-mac cells (CD45+CD11b+CD86+) and Pro-mac cells (CD45+CD11b+ARG +) and sorted them by flow cytometry. The proportion of Pro-mac cells in LUAD tissues increased significantly after neoadjuvant chemotherapy. Pro-mac cells promote tumor growth and angiogenesis and also suppress tumor immunity. Moreover, by analyzing the remodeling of T and B cells induced by neoadjuvant therapy, we noted that chemotherapy ignited a relatively more robust immune cytotoxic response toward tumor cells. Our study demonstrates that chemotherapy induces metabolic reprogramming within the tumor microenvironment of LUAD, particularly affecting the function and composition of immune cells such as macrophages and T cells. We believe our findings will offer insight into the mechanisms of drug resistance and provide novel therapeutic targets for LUAD in the future.
化疗被广泛用于综合治疗肺腺癌(LUAD)患者。鉴于化疗因耐药性和其他问题存在局限性,探索化疗和免疫疗法在这些方面的影响至关重要。在本研究中,对9例LUAD患者的肿瘤样本进行了单细胞RNA测序(scRNA-seq)分析,其中4例仅接受了手术,5例接受了新辅助化疗。进行了体外和体内实验,包括流式细胞术、免疫荧光、海马实验和肿瘤异种移植模型,以验证我们的发现。总共83622个细胞被纳入后续分析。不同组之间细胞类型的组成表现出高度异质性。功能富集分析表明,化疗在肿瘤细胞和巨噬细胞中驱动了显著的代谢重编程。我们鉴定出两种巨噬细胞亚型:抗巨噬细胞(CD45+CD11b+CD86+)和促巨噬细胞(CD45+CD11b+ARG+),并通过流式细胞术对它们进行了分选。新辅助化疗后,LUAD组织中促巨噬细胞的比例显著增加。促巨噬细胞促进肿瘤生长和血管生成,还抑制肿瘤免疫。此外,通过分析新辅助治疗诱导的T细胞和B细胞重塑,我们注意到化疗引发了对肿瘤细胞相对更强有力的免疫细胞毒性反应。我们的研究表明,化疗在LUAD的肿瘤微环境中诱导代谢重编程,尤其影响巨噬细胞和T细胞等免疫细胞的功能和组成。我们相信我们的发现将为耐药机制提供见解,并在未来为LUAD提供新的治疗靶点。