Abstract
Long non‑coding RNAs (lncRNAs) have been discovered to serve important roles in a variety of types of cancer, including cervical cancer. The low expression of lncRNA long intergenic non‑protein coding RNA 861 (LINC00861) is related to poor prognosis in ovarian cancer. However, the effects and underlying mechanisms of LINC00861 in cervical cancer remain largely unknown. The present study aimed to examine the role of LINC00861 in the development and progression of ovarian cancer and its underlying mechanisms. The expression levels of LINC00861 and microRNA (miR)‑513b‑5p were analyzed using reverse transcription‑quantitative PCR analysis. Cell proliferation, migration and invasion were measured by using Cell Counting Kit‑8, colony formation, wound healing and Transwell assays, respectively. A luciferase assay was used to determine whether miR‑513b‑5p targeted LINC00861 and PTEN. The expression of protein was measured by using western blot assay. The results of the present study discovered that LINC00861 expression levels were significantly downregulated in cervical cancer tissues and CaSki and ME‑180 cell lines. Downregulated LINC00861 expression levels were identified to be associated with an advanced‑stage, lymph node metastasis and the poor survival of patients with cervical cancer. Gene Set Enrichment Analysis revealed that the PI3K/AKT/mTOR signaling pathway was significantly enriched in cervical tumors expressing low expression levels of LINC00861 compared with tumors expressing high levels of LINC00861. The overexpression of LINC00861 reduced cervical cancer cell proliferation, migration, invasion and epithelial‑mesenchymal transition (EMT) processes, upregulated PTEN protein expression levels and downregulated phosphorylated (p)‑AKT and p‑mTOR protein expression levels. The regulatory relationship between LINC00861, microRNA (miR)‑513b‑5p and PTEN was validated using a dual luciferase reporter gene assay. PTEN expression levels were significantly downregulated in the miR‑513b‑5p mimic group and significantly upregulated in the miR‑513b‑5p inhibitor group compared with the mimic NC and inhibitor NC in both cell lines. Furthermore, LINC00861 was suggested to serve as a competing endogenous RNA by sponging miR‑513b‑5p and consequently upregulating the expression levels of PTEN in cervical cancer cells. The expression of PTEN, the phosphorylation of Akt and mTOR and and the EMT phenotype were rescued following co‑transfection with LINC00861 and miR‑513b‑5p mimics. In conclusion, the findings of the present study indicated that the LINC00861/miR‑513b‑5p axis may inhibit the progression of cervical cancer cells through the PTEN/AKT/mTOR signaling pathway to suppress the EMT process.