By analyzing the cellular communication between primary and secondary tumor microenvironments, we delineate the specific roles and mechanisms of Cav-1 in lung metastasis of BC by focusing on the formation of PMN, which could increase the expression of PMN-related genes in lung epithelial cells, promote ECM deposition in lung fibroblasts and facilitate the M2 polarization of lung macrophages. The gene discussed is CAV1; the disease is neoplasm.