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Figure 2. 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.