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Cancer-associated fibroblast-derived extracellular vesicles deliver ATP6V1C1 to promote lung adenocarcinoma metastasis via the ID1-IGFBP3 axis

Chen et al. reveal the V-ATPase subunit ATP6V1C1 as a non-canonical transcriptional repressor delivered by CAF-derived EVs to drive LUAD metastasis. By suppressing IGFBP3, ATP6V1C1 simultaneously triggers EMT and amplifies stromal IGF1 signaling, creating a potent pro-metastatic feedforward loop.

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