Abstract: Objective: LINC00657 has been observed to be aberrantly expressed in a variety of cancers. Despite this, the precise expression patterns and functions of LINC00657 in cervical cancer remain elusive. Therefore, the roles and underlying mechanisms of LINC00657 in cervical cancer were investigated in this study. Methods: Bioinformatics analysis predicted potential binding sites between LINC00657 and miR-30a-5p and between miR-30a-5p and Skp2, which were verified using RNA immunoprecipitation and dual-luciferase reporter experiments. LINC00657, miR-30a-5p, and Skp2 expression levels in cervical cancer tissues and cell lines were assessed using RT-qPCR. Additionally, western blotting was used to examine the protein level of Skp2 in cells and subcutaneous xenograft tumor models in nude mice. Immunohistochemistry was used to analyze Skp2 expression in animal tissues. Cellular processes of cervical cancer cell lines were evaluated using CCK8, scratch, and Transwell assays. Results: LINC00657 and Skp2 presented binding sites for miR-30a-5p. In cervical cancer, LINC00657 and Skp2 showed high expression, while miR-30a-5p displayed low expression. LINC00657 was confirmed as a regulator of Skp2 expression, and miR-30a-5p was shown to target Skp2. Conclusion: The role of LINC00657 as a "molecular sponge" was evident, adsorbing miR-30a-5p and thereby upregulating Skp2 to promote cervical cancer progression.