FOXP3‑induced LINC00885 promotes the proliferation and invasion of cervical cancer cells
- Yawen Liu
- Haiyan Tu
- Lingling Zhang
- Jianping Xiong
- Ling Li
Affiliations: Medical College of Nanchang University, Nanchang, Jiangxi 330006, P.R. China, Department of Gynecological Oncology, Jiangxi Maternal and Child Health Hospital, Nanchang, Jiangxi 330006, P.R. China, Department of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China
- Published online on: April 16, 2021 https://doi.org/10.3892/mmr.2021.12097
Copyright: © Liu
et al. This is an open access article distributed under the
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Cervical cancer (CC) is the fourth most common type of cancer in women worldwide. LINC00885, a novel oncogenic type of long non‑coding RNA, is upregulated in various types of cancer, but its expression in CC remains unknown. The aim of the present study was to investigate the expression of LINC00885 in CC, and its effect on the proliferation and invasion of CC cells in vitro. The expression levels of LINC00885 and forkhead box protein 3 (FOXP3) from The Cancer Genome Atlas (TCGA) were selected to analyze the differences between CC tissues and normal cervical tissues using bioinformatics analyses. Reverse transcription‑quantitative (RT‑q)PCR was used to detect the relative expression of LINC00885 in CC cell lines, and its expression was knocked down. Cell Counting Kit‑8 assays and EdU staining were used to detect the changes in cell proliferative capacity of cells. Transwell experiments were used to examine cell invasion. Dual‑luciferase reporter and chromatin immunoprecipitation assays were performed to examine the interactions between LINC00885 and FOXP3. FOXP3 and epithelial‑mesenchymal transition (EMT)‑related proteins were detected using western blotting. The expression of LINC00885 and FOXP3 in CC tissues and CC cells was significantly higher compared with the normal cervical tissues and normal cervical epithelial cells. FOXP3 could specifically interact with the promoter of LINC00885 and activate LINC00885 transcription. Knockdown of LINC00885 and silencing of FOXP3 significantly inhibited proliferation, invasion and EMT of CC cells. Overexpression of LINC00885 reversed the inhibitory effects of FOXP3 knockdown on the proliferation and invasion of CC cells. Collectively, LINC00885 and FOXP3 may serve as biomarkers for the early diagnosis of CC and as a potential therapeutic target for reversing the malignant phenotype of CC.