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. 2024 Sep 10;7:32. doi: 10.20517/cdr.2024.55

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© The Author(s) 2024.

© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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The origin of CAFs and their crosstalk signaling pathways regulating tumor microenvironment. (A) CAFs in lung cancer are potentially derived from tissue-resident fibroblasts, mesenchymal stem cells, epithelial cells, and pericytes; (B) These CAFs modulate the tumor microenvironment by activating a variety of signaling pathways, including TGF-β, Wnt/β-catenin, MAPK, IL6, EGFR, JAK/STAT, and NF-κB, resulting in the orchestration of processes such as proliferation and ECM remodeling, immunosuppression, EMT, drug resistance, and angiogenesis. CAFs: Cancer-associated fibroblasts; TGF-β: transforming growth factor beta; MAPK: mitogen-activated protein kinases; IL: interleukin; EGFR: epidermal growth factor receptor; JAK/STAT: Janus kinases/signal transducers and activators of transcription; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; ECM: extracellular matrix, EMT: epithelial-mesenchymal transition.