一种用于克服非小细胞肺癌治疗中抗原异质性的多靶向 CAR-T 细胞平台
A Multi-Targeting Chimeric Antigen Receptor-T Cell Platform to Overcome Antigen Heterogeneity in the Treatment of Non-Small Cell Lung Cancer.
这些发现支持采用多靶点CAR-T 策略来应对NSCLC及可能其他实体瘤中的抗原异质性。
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
基于生物信息学与实验方法分析肺腺癌与肺鳞状细胞癌中 LATS2 的表达差异
英文原题：LATS2 expression differences in lung adenocarcinoma and lung squamous cell carcinoma analyzed using bioinformatics and experimental approaches.
查看英文原题
LATS2 expression differences in lung adenocarcinoma and lung squamous cell carcinoma analyzed using bioinformatics and experimental approaches.
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中文摘要
本研究旨在考察大肿瘤抑制激酶2（LATS2）在肺腺癌（LUAD）和肺鳞状细胞癌（LUSC）中的作用及表达。研究者利用癌症基因组图谱（TCGA）数据分析LATS2在LUAD和LUSC中的表达及其与临床特征和患者生存的关系。筛选100个LATS2相关基因，进行京都基因与基因组百科全书（KEGG）及基因本体（GO）富集分析；并分析LATS2表达与免疫细胞浸润，尤其是CD4⁺和CD8⁺TIL（肿瘤浸润淋巴细胞）的关系。通过观察LATS2过表达后LUAD和LUSC细胞增殖、凋亡、迁移和侵袭的变化，验证其在肿瘤细胞中的作用。LUAD和LUSC中LATS2表达均较低。在LUAD中，LATS2高表达与淋巴结转移、远处转移和TNM分期相关，并且是总生存期和无进展生存期的独立风险因素。相比之下，LUSC中LATS2与临床特征和生存的关联较弱。LUAD和LUSC中的LATS2相关基因在相关功能通路和生物过程方面存在差异。在LUAD中，LATS2与CD4⁺ TIL比例及CD4⁺/CD8⁺ TIL比例呈正相关，与CD8⁺ TIL比例呈负相关；LUSC中未观察到此类关联。体外实验显示，LATS2过表达可抑制LUAD和LUSC细胞系的增殖、迁移及侵袭，并促进凋亡，且在LUAD细胞中的作用更强。
总之，LATS2在LUAD和LUSC中均发挥肿瘤抑制作用。在LUAD中，LATS2是患者生存的独立风险因素，这可能与其和CD8⁺ TIL水平密切相关；但这一关系在LUSC中并不明显。
展开英文摘要原文
The present study aimed to investigate the role and expression of large tumor suppressor kinase 2 (LATS2) in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). The expression levels of LATS2 in LUAD and LUSC, as well as their association with clinical characteristics and patient survival, were analyzed using data obtained from The Cancer Genome Atlas. A total of 100 LATS2-related genes were screened to conduct Kyoto Encyclopedia of Genes and Genomes and Gene Ontology enrichment analyses. The association between LATS2 expression and immune cell infiltration, particularly CD4 + and CD8 + tumor-infiltrating lymphocytes (TILs), was analyzed. The role of LATS2 in tumor cells was validated by observing the changes in proliferation, apoptosis, migration and invasion of LUAD and LUSC cells following LATS2 overexpression. LATS2 expression was low in both LUAD and LUSC.
In LUAD, high expression of LATS2 was associated with lymph node metastasis, distant metastasis and TNM stage and served as an independent risk factor for both overall survival and progression-free survival. Conversely, in LUSC, LATS2 exhibited a weak association with clinical characteristics and survival. In LUAD and LUSC, LATS2-related genes exhibited differences in their associated functional pathways and biological processes.
In LUAD, LATS2 was positively associated with CD4 + TIL proportions and CD4 + /CD8 + TIL proportions, while exhibiting a negative association with CD8 + TIL proportions. In LUSC, no such associations were observed. In vitro experiments demonstrated that overexpression of LATS2 inhibited proliferation, migration and invasion, while promoting apoptosis, in both LUAD and LUSC cell lines, with notably stronger effects observed in LUAD cells.
In conclusion, LATS2 exerts tumor-suppressive functions in both LUAD and LUSC. In LUAD, LATS2 is an independent risk factor for patient survival, possibly due to its close association with CD8 + TIL levels; however, this relationship is not pronounced in LUSC.
论文信息
- 作者
- Zhang Z、Zhang S、Xu Y、Zhang C、Zhang X
- 单位
- Department of Oncology Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China.China
- 期刊
- Oncology letters2026 Jul
- 原文标识
- PubMed 42272771 · DOI 10.3892/ol.2026.15671
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