Long non-coding RNAs (lncRNAs) play important roles in tumor progression. Recently, increasing evidence showed that lncRNA NORAD could be used as an important regulator in tumor progression. However, the roles and underlying mechanism of NORAD in cervical cancer (CC) remain unclear. In the present study, we found that NORAD expression was significantly up-regulated in CC tissues and cell lines. High NORAD expression was correlated with advanced FIGO stage, lymph nodes metastasis, vascular invasion, and poor overall survival of CC patients. In vitro function assays, we showed that NORAD suppression reduced CC cells proliferation, invasion, and epithelial-mesenchymal transition (EMT) processes. Furthermore, the underlying mechanism studies showed that lncRNA NORAD could sponge miR-590-3p to promote the proliferation and invasion of CC cells via upregulating SIP1 expression. In addition, we showed that NORAD inhibition could reduce CC cells growth in vivo. Taken together, these results suggested that NORAD could serve as a ceRNA in CC progression by modulating miR-590-3p/SIP1 axis and act as a therapeutic target for the treatment of CC.