Ror2 signaling regulates Golgi structure and transport through IFT20 for tumor invasiveness. Ror2, a receptor tyrosine kinase, promotes invadopodia formation, which is essential for tumor invasion. This study identifies IFT20 as a new target of Ror2 signaling in tumors lacking primary cilia. IFT20 mediates Ror2's ability to induce tumor invasiveness by regulating Golgi structure and transport. IFT20 affects the GM130-AKAP450 complex, promoting Golgi ribbon formation and polarized secretion for cell migration and invasion. IFT20 also enhances transport efficiency through the Golgi complex. These findings reveal how Ror2 signaling promotes tumor invasiveness and advance understanding of Golgi structure and transport regulation. Ror2 signaling activates non-canonical Wnt pathways, including Dishevelled, JNK, and c-Src, and inhibits the β-catenin-dependent pathway. In tumors, Ror2 signaling is constitutively active, promoting EMT and MMP-13 expression, which degrade the extracellular matrix to facilitate invasion. IFT20 is localized at the Golgi and is involved in Golgi ribbon formation and MT nucleation. It also plays a role in non-ciliary functions, such as endocytic recycling in T cells and ER-to-Golgi transport in osteoblasts. IFT20 regulates Golgi structure and transport by modulating the GM130-AKAP450 complex and promoting anterograde Golgi transport. These findings highlight the role of IFT20 in mediating Ror2 signaling to promote tumor invasiveness and invadopodia formation. The study also shows that IFT20 is required for Golgi ribbon formation and MT nucleation, and its loss disrupts Golgi structure and transport. The results suggest that IFT20 is essential for tumor invasiveness and that its function in Golgi structure and transport is critical for Ror2 signaling. The study provides new insights into the mechanisms by which Ror2 signaling promotes tumor invasiveness and advances understanding of Golgi structure and transport regulation.Ror2 signaling regulates Golgi structure and transport through IFT20 for tumor invasiveness. Ror2, a receptor tyrosine kinase, promotes invadopodia formation, which is essential for tumor invasion. This study identifies IFT20 as a new target of Ror2 signaling in tumors lacking primary cilia. IFT20 mediates Ror2's ability to induce tumor invasiveness by regulating Golgi structure and transport. IFT20 affects the GM130-AKAP450 complex, promoting Golgi ribbon formation and polarized secretion for cell migration and invasion. IFT20 also enhances transport efficiency through the Golgi complex. These findings reveal how Ror2 signaling promotes tumor invasiveness and advance understanding of Golgi structure and transport regulation. Ror2 signaling activates non-canonical Wnt pathways, including Dishevelled, JNK, and c-Src, and inhibits the β-catenin-dependent pathway. In tumors, Ror2 signaling is constitutively active, promoting EMT and MMP-13 expression, which degrade the extracellular matrix to facilitate invasion. IFT20 is localized at the Golgi and is involved in Golgi ribbon formation and MT nucleation. It also plays a role in non-ciliary functions, such as endocytic recycling in T cells and ER-to-Golgi transport in osteoblasts. IFT20 regulates Golgi structure and transport by modulating the GM130-AKAP450 complex and promoting anterograde Golgi transport. These findings highlight the role of IFT20 in mediating Ror2 signaling to promote tumor invasiveness and invadopodia formation. The study also shows that IFT20 is required for Golgi ribbon formation and MT nucleation, and its loss disrupts Golgi structure and transport. The results suggest that IFT20 is essential for tumor invasiveness and that its function in Golgi structure and transport is critical for Ror2 signaling. The study provides new insights into the mechanisms by which Ror2 signaling promotes tumor invasiveness and advances understanding of Golgi structure and transport regulation.