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肺腺癌肿瘤微环境的细胞成分：小分子化合物的潜在靶点。

Cell components of tumor microenvironment in lung adenocarcinoma: Promising targets for small-molecule compounds.

作者信息

Han Mingyu, Wan Feng, Xiao Bin, Du Junrong, Peng Cheng, Peng Fu

机构信息

Key Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu, Sichuan 610041, China.

State Key Laboratory of Southwestern Chinese Medicine Resources, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610075, China.

出版信息

Chin Med J (Engl). 2025 Apr 20;138(8):905-915. doi: 10.1097/CM9.0000000000003341. Epub 2024 Nov 8.

DOI:10.1097/CM9.0000000000003341
PMID:39512221
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12037101/
Abstract

Lung cancer is one of the most lethal tumors in the world with a 5-year overall survival rate of less than 20%, mainly including lung adenocarcinoma (LUAD). Tumor microenvironment (TME) has become a new research focus in the treatment of lung cancer. The TME is heterogeneous in composition and consists of cellular components, growth factors, proteases, and extracellular matrix. The various cellular components exert a different role in apoptosis, metastasis, or proliferation of lung cancer cells through different pathways, thus contributing to the treatment of adenocarcinoma and potentially facilitating novel therapeutic methods. This review summarizes the research progress on different cellular components with cell-cell interactions in the TME of LUAD, along with their corresponding drug candidates, suggesting that targeting cellular components in the TME of LUAD holds great promise for future theraputic development.

摘要

肺癌是世界上最致命的肿瘤之一，其5年总生存率低于20%，主要包括肺腺癌（LUAD）。肿瘤微环境（TME）已成为肺癌治疗的新研究热点。TME的组成具有异质性，由细胞成分、生长因子、蛋白酶和细胞外基质组成。各种细胞成分通过不同途径在肺癌细胞的凋亡、转移或增殖中发挥不同作用，从而有助于腺癌的治疗并可能促进新的治疗方法。本综述总结了LUAD的TME中不同细胞成分及其细胞间相互作用的研究进展，以及相应的候选药物，表明针对LUAD的TME中的细胞成分在未来治疗发展中具有巨大潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a3/12037101/c7e48d8e1d8e/cm9-138-0905-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a3/12037101/bfe910c61f17/cm9-138-0905-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a3/12037101/292ff1d99677/cm9-138-0905-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a3/12037101/c7e48d8e1d8e/cm9-138-0905-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a3/12037101/bfe910c61f17/cm9-138-0905-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a3/12037101/292ff1d99677/cm9-138-0905-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24a3/12037101/c7e48d8e1d8e/cm9-138-0905-g003.jpg

相似文献

[1]
Cell components of tumor microenvironment in lung adenocarcinoma: Promising targets for small-molecule compounds.

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引用本文的文献

[1]
Integrative Multi-Omics Analysis Reveals the Molecular Characteristics, Tumor Microenvironment, and Clinical Significance of Ubiquitination Mechanisms in Lung Adenocarcinoma.

Int J Mol Sci. 2025-7-6

[2]
Clinical significance and biological function of PRKCQ-AS1/miR-582-3p expression in LUAD.

Hereditas. 2025-7-1

[3]
Expression of PSMD14 in lung adenocarcinoma and its impact on immune cell infiltration and prognosis: a comprehensive analysis based on RNA and single-cell RNA sequencing.

Front Immunol. 2025-5-22

本文引用的文献

[1]
Combination of IL-33 with PD-1 blockade augment mILC2s-mediated anti-tumor immunity.

Cancer Immunol Immunother. 2024-3-2

[2]
High FLT3 expression increases immune-cell infiltration in the tumor microenvironment and correlates with prolonged disease-free survival in patients with non-small cell lung cancer.

Mol Oncol. 2024-5

[3]
Neutrophil infiltration associated genes on the prognosis and tumor immune microenvironment of lung adenocarcinoma.

Front Immunol. 2023

[4]
PKM2 is a potential prognostic biomarker and related to immune infiltration in lung cancer.

Sci Rep. 2023-12-14

[5]
Circ_16601 facilitates Hippo pathway signaling via the miR-5580-5p/FGB axis to promote my-CAF recruitment in the TME and LUAD progression.

Respir Res. 2023-11-12

[6]
Comprehensive bioinformatics analysis of the solute carrier family and preliminary exploration of SLC25A29 in lung adenocarcinoma.

Cancer Cell Int. 2023-9-29

[7]
Exo-miR-1290-induced by COX-2 overexpression promotes cancer-associated fibroblasts activation and tumor progression by CUL3-Nrf2 pathway in lung adenocarcinoma.

Cell Commun Signal. 2023-9-18

[8]
COL3A1-positive endothelial cells influence LUAD prognosis and regulate LUAD carcinogenesis by NCL-PI3K-AKT axis.

J Gene Med. 2024-1

[9]
Activation of the GPR35 on ILC2 drives immunosuppression to promote lung cancer progression.

Am J Cancer Res. 2023-6-15

[10]
B4GALT1 promotes immune escape by regulating the expression of PD-L1 at multiple levels in lung adenocarcinoma.

J Exp Clin Cancer Res. 2023-6-12

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