Regulation of Golgi morphology states in cancer. The Golgi oscillates dynamically between three main defined morphological states: the condensed (left Golgi), the elongated (middle Golgi), or the fragmented (right Golgi). Zeb1-mediated EMT orchestrates Golgi condensation by repressing the epithelial miRNA, namely, miR-200, and upregulating PAQR11. PAQR11 is a Golgi scaffold protein that mediates Golgi organization and secretion of pro-metastatic factors. The elongated Golgi morphology is maintained via the PITPNC1–RAB1B–GOLPH3–MYO18A complex, where GOLPH3 links vesicles to myosin motors and facilitates movement along actin filaments. Additionally, other Golgi matrix proteins, namely, GM130 and GRASP65, also interact with various Golgi factors to promote the elongated ribbon-like structures, which is necessary for cancer cell invasion and vesicular trafficking. Loss of these matrix proteins prevents organelle stacking, thereby leading to a fragmented Golgi architecture, which is commonly seen during mitosis. Moreover, in prostate cancer, a disrupted Golgi promotes invasion through dysregulated vesicle interaction with RAB6A, which results in diminished interactions with myosin, MYOIIA, and fewer fusion events.