Recent multi-omics research demonstrates that pancreatic cancer cachexia is driven by the spatial organization of a pathogenic niche consisting of SEMA4A-expressing tumor cells, AQP9-positive macrophages, and LOXL2-secreting cancer-associated fibroblasts. Within this localized microenvironment, tumor-derived bone morphogenetic protein-2 reprograms macrophages, which subsequently release chemokines that activate fibroblasts to produce N-glycosylated LOXL2. This paracrine signaling loop reinforces tumor signaling pathways and promotes severe systemic skeletal muscle wasting. Furthermore, clinical analyses reveal that the molecular signatures of this tri-cellular niche can successfully predict postoperative weight loss and new-onset cachexia in patients.
References:
Hu Y, Lv G, Yuan H, et al. Spatial evolution of a cachexia-promoting microenvironment in pancreatic cancer[J]. Cell, 2026.
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