Cav1 and Gal-3 in tumor progression. (1) In cells lacking the galectin lattice, Cav1 scaffolds recruit receptors and inhibit signaling. (2) Loss of Cav1 enables receptor signaling, promoting tumor cell proliferation and tumor growth. (3) Expression of Mgat5-branched N-glycans and Gal-3 and receptor recruitment to the galectin lattice limits receptor down-regulation via endocytosis, and promotes signaling potential. (4) Receptor sequestration by the galectin lattice overrides Cav1 suppressor activity, enabling elevated Cav1 expression in advanced tumors. Gal-3 and pY14Cav1 work together to promote focal adhesion turnover and enhance FAK activation, tumor cell migration, and metastasis. Competitive and coordinate action between Cav1 scaffolds and the galectin lattice at various stages of tumor progression may explain how Cav1 can act as both a tumor promoter and suppressor.