Long noncoding RNAs (lncRNAs) have been associated with cervical cancer (CC), but molecular mechanisms behind the specific correlation with cervical carcinogenesis have not been fully understood. In this study, the expression level of IncRNA MIR205HG in CC cells was determined by qRT-PCR. In vitro functional assays (CCK-8 assay, EdU incorporation assay, apoptotic assays, Transwell assay, wound-healing assay) were performed to investigate the biological effects of MIR205HG ectopic expression on CC cells. RNA Immunoprecipitation (RIP), RNA pulldown, and Dual-luciferase reporter assay were employed to examine the interaction among MIR205HG, miR-122-5p, and FOXP2. Rescue experiments were performed to explore whether MIR205HG regulates tumor development via upregulating FOXP2. Conclusively, we found that MIR205HG was upregulated in cervical cancer tissues supported by GEPIA database and in cell lines through qRT-PCR, and its depletion inhibited the proliferation and metastasis of CC cells. Furthermore, MIR205HG could sponge miR-16-5p to accelerate malignant progression of CC cells via upregulating FOXP2. Conclusively, these results demonstrated that MIR205HG could serve as a ceRNA in CC progression by modulating miR-122-5p/FOXP2 axis and exert a pro-tumorigenesis function, which may be a novel therapeutic target for diagnosis and the treatment of CC. (C) 2019 Elsevier Inc. All rights reserved.