Long non-coding RNA urothelial carcinoma associated 1 (lncRNA UCA1) promotes cancer progression and enhances chemoresistance through miR-204-5p in a few cancers. However， no studies have investigated whether UCA1 regulates glioma metastasis through miR-204-5p and its target. In the present study， cell migration， invasion and epithelial-mesenchymal transition (EMT) were evaluated in glioma cells overexpressing UCA1. The relationships among UCA1， miR-204-5p and ZEB1 were examined by real-time PCR， western blotting and dual-luciferase reporter assays. The effect of UCA1 knockdown on xenograft tumor growth was investigated. The levels of miR-204-5p， fibronectin， COL5 A1 and ZEB1 in tumor tissues were also determined. The results showed that UCA1 overexpression promoted cell migration， invasion and EMT. UCA1 interacted with miR-204-5p and decreased its level. ZEB1 was identified as a direct target of miR-204-5p and miR-204-5p negatively regulated ZEB1 expression. Moreover， UCA1 sponged miR-204-5p and partially rescued the inhibitory effect of miR-204-5p on ZEB1. In our in vivo studies， UCA1 knockdown reduced tumor volume and tumor weight. In addition， the levels of fibronectin， COL5 A1 and ZEB1 were decreased， while miR-204-5p level was increased. The present study provides the first evidence that UCA1 promotes glioma metastasis through the miR-204-5p/ZEB1 axis， contributing to the understanding of the pathogenesis of glioma.