Randomized trial examines invadopodia formation in triple-negative breast cancer, suggesting novel tumor-adipocyte interactions.
Key Points
This research aims to elucidate the role of cancer-associated adipomes in enhancing metastatic potential and invadopodia formation in triple-negative breast cancer.
Isolated large (L)-adipomes from TNBC patient plasma and tumor-associated mammary fat using a murine TNBC model (EO771-C57BL/6).
Conducted integrated transcriptomic and proteomic analyses to investigate the effects of L-adipomes on TNBC cell behavior.
Circulating L-adipomes from metastatic TNBC subjects induced epithelial-to-mesenchymal transition (EMT) and stemness signaling in non-tumorigenic breast cells.
TAMF-derived L-adipomes from metastatic mice promoted transcriptional and functional reprogramming in murine TNBC cells, enriched in phospholipids.
Adipomes activated MAPK signaling pathways, upregulating proteins related to actin remodeling and extracellular matrix degradation.