Increasing evidences have proven that long non-coding RNA (lncRNA) has a vital impact on the procession of cervical cancer (CC). This study aims at investigating the clinical significance of LINC01089 in CC and exploring its biological functions and potential molecular mechanisms. Quantitative real time polymerase chain reaction (qRT-PCR) was utilized to investigate the expressions of LINC01089 and miR-27a-3p in CC cells and tissues. Analysis of the correlation between the expression level of LINC01089 and the clinical pathological parameters of CC was then conducted. The human CC cell lines HeLa and SiHa were utilized for transfection to establish gain-of-function model and loss-of-function models. Western blot and qRT-PCR were performed to detect B-cell translocation gene-2 (BTG2) expression in CC cells. Cell counting kit-8 (CCK-8) method and 5-Bromo-2-deoxyUridine (BrdU) assay were performed to detect the proliferation of CC cells. Transwell method was employed to evaluate the migration and invasion of CC cells. The interactions between LINC01089 and miR-27a-3p were verified by bioinformatics, dual luciferase reporter gene experiment and RIP experiment, respectively. The expression of LINC01089 in CC was markedly down-regulated. The low expression of LINC01089 in CC was closely associated with larger tumor size and positive lymph node metastasis. Moreover, overexpression of LINC01089 impeded the proliferation and metastasis of CC cells, whereas knockdown of LINC01089 had opposite biological functions. In terms of mechanism, LINC01089 could sponge miR-27a-3p and indirectly up-regulate BTG2 expression. LINC01089, as a tumor suppressor, impedes the development of CC by targeting miR-27a-3p to upregulate BTG2 expression. This article is protected by copyright. All rights reserved.