ArticleMolecular medicine reports2021
Mechanism underlying long non‑coding RNA ILF3‑AS1‑mediated inhibition of cervical cancer cell proliferation, invasion and migration, and promotion of apoptosis.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 3 citations in OpenAlex.
- Review
- The expression profiling of serum circPHLPP2 and LncRNA ILF3 in colorectal cancer patients.Scientific reports · 2026Article
- Computational Resources for Studying miRNA-lncRNA Interactions.Methods in molecular biology (Clifton, N.J.) · 2026Article
- LncRNA DNAJC3-AS1 promotes gastric cancer malignancy through miR-576-5p-mediated upregulation of LYPLA1.American journal of cancer research · 2026Article
- Review
- Overexpression of miR-3653 is Associated with HPV Infection and Serves as a Biomarker in Patients with Cervical Cancer.International journal of women's health · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non‑coding RNA ILF3 divergent transcript (ILF3‑AS1) displays a tumor‑suppressing effect. StarBase predicted that the potential target microRNA (miR) of ILF3‑AS1 was miR‑454‑3p; therefore, the present study investigated the effect of ILF3‑AS1 and its target miR‑454‑3p on cervical cancer (CC). Gene Expression Profiling Interactive Analysis was used to predict the expression of ILF3‑AS1 in CC and the overall survival rate of patients. The present study demonstrated that ILF3‑AS1 expression was significantly downregulated in human CC tissues and cells compared with adjacent tissues (ANTs) and normal cervical epithelial cells (NCEs), respectively. Patients with CC with high ILF3‑AS1 expression displayed higher survival rates compared with patients with low ILF3‑AS1 expression. Cell viability, apoptosis, migration and invasion were detected by performing Cell Counting Kit‑8, flow cytometry, wound healing and Transwell assays, respectively. Compared with the negative control (NC) group, ILF3‑AS1 overexpression significantly inhibited CC cell viability and migration, but significantly increased CC cell apoptosis. Moreover, ILF3‑AS1 overexpression significantly upregulated E‑Cadherin expression levels, but significantly downregulated N‑Cadherin and snail family transcriptional repressor 1 expression levels compared with the NC group. miR‑454‑3p expression was negatively correlated with ILF3‑AS1, and highly expressed in CC tissues and cells compared with ANTs and NCEs, respectively. PTEN, which was predicted and verified as the target gene for miR‑454‑3p, was significantly downregulated in CC tissues and cells compared with ANTs and NCEs, respectively. ILF3‑AS1 expression was positively correlated with PTEN expression, and ILF3‑AS1 overexpression partially reversed the inhibitory effect of miR‑454‑3p on PTEN expression. In conclusion, the present study indicated that ILF3‑AS1 inhibited CC cell proliferation and migration, and promoted CC cell apoptosis by inhibiting epithelial‑mesenchymal transition, and ILF3‑AS1 overexpression partially reversed the inhibitory effect of miR‑454‑3p on PTEN expression.
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