ArticleDiscover oncology2026
Exosomal miR-484 from lung adenocarcinoma promotes osteoclastogenesis and osteolytic bone metastasis by targeting PECAM1.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Bone metastasis is a frequent and devastating complication in lung adenocarcinoma (LUAD), where excessive osteoclast activation drives osteolytic destruction and skeletal-related events. How tumor-derived exosomes reprogram osteoclast precursors to establish a bone-metastatic niche remains incompletely understood. Here, we identify an exosomal miR-484–platelet endothelial cell adhesion molecule-1 (PECAM1) axis that links LUAD to pathological osteoclastogenesis and osteolytic bone metastasis. Using a highly bone-tropic Lewis lung carcinoma (BM-LLC) model, we show that BM-LLC-derived exosomes are preferentially internalized by osteoclast precursors and are markedly enriched in miR-484. Exosomal transfer of miR-484 increases intracellular miR-484 in these precursor cells and directly suppresses PECAM1, a negative regulator of osteoclastogenesis. PECAM1 repression activates NFATc1 and c-Fos, up-regulates osteoclast markers (TRAP, CTSK, RANK), and promotes osteoclast differentiation and bone matrix degradation in vitro. Gain- and loss-of-function studies demonstrate that PECAM1 overexpression or miR-484 inhibition attenuates BM-LLC exosome–induced osteoclastogenesis, whereas PECAM1 knockdown phenocopies miR-484 and further amplifies osteoclast activation. In vivo, systemic administration of BM-LLC exosomes exacerbates osteolytic lesions and bone tumor burden without altering lung colonization, while therapeutic delivery of antagomiR-484 partly restores PECAM1 expression, suppresses osteoclastogenic signaling, and alleviates bone loss. Circulating exosomal miR-484 levels correlate with the severity of osteolysis, supporting its potential as a liquid biopsy biomarker. Collectively, our data define exosomal miR-484–mediated PECAM1 suppression as a critical mechanism by which LUAD cells remodel the bone microenvironment, and highlight the miR-484–PECAM1axis as a tractable target for preventing or treating osteolytic bone metastasis.
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