Cervical cancer has the second highest incidence rate among cancers in females, accounting for a majority of cancer-related deaths globally. However, the mechanism of cervical cancer pathogenesis is still unclear. UCA1 is considered an oncogene that can transcribe into a long noncoding RNA (lncRNA). This study aimed to determine the function of UCA1 in cervical cancer. A series of experiments involving BrdU, MTS, scratch-adhesion test, and cell invasion assays were conducted to determine the cellular capabilities of proliferation, viability, migration, and invasion, respectively. Binding sites between UCA1 and miR-143 were identified using a luciferase reporter system, whereas mRNA and protein expression of target genes was determined by RT-PCR and immunoblot, respectively. The results shown that the upregulation of lncRNA UCA1 was found in human cervical cancer. Interference of lncRNA UCA1 inhibited cell proliferation, migration, invasion, and viability. Results of the luciferase reporter assay revealed a binding site between lncRNA UCA1 and miR-206. Knockdown of lncRNA UCA1 could directly upregulate miR-206 expression. VEGF downregulation was also observed after knockdown of lncRNA UCA1. Moreover, co-transfection of anti-miR-206 oligodeoxyribonucleotide (AMO-206) in cervical cancer cells reversed the effect of lncRNA UCA1 on VEGF. Therefore, we concluded that LncRNA UCA1 is upregulated in cervical cancer, and its knockdown can upregulate miR-206, thus, suppressing the growth of cervical cancer cells. LncRNA UCA1 is a potential target in cervical cancer treatment.