Functionally, as secreted protein, we showed that autocrine ANGPTL4 promoted TNBC cell proliferation and metastasis by activating the integrin/JAK2/STAT3 pathway, while paracrine ANGPTL4 triggered protumoral macrophage polarization within the tumor-associated microenvironment, thereby contributing to TNBC progression. Here, ANGPTL4 is linked to neoplasm.