Mechanism underlying long non‑coding RNA ILF3‑AS1‑mediated inhibition of cervical cancer cell proliferation, invasion and migration, and promotion of apoptosis

Mol Med Rep. 2021 Aug;24(2):554. doi: 10.3892/mmr.2021.12193. Epub 2021 Jun 3.

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.

Keywords: PTEN; cervical cancer; lncRNA ILF3 divergent transcript; microRNA‑454‑3p.

MeSH terms

  • Adult
  • Apoptosis / genetics
  • Cell Line
  • Cell Movement / genetics
  • Cell Proliferation / genetics
  • Databases, Genetic
  • Down-Regulation / genetics
  • Epithelial-Mesenchymal Transition / genetics
  • Female
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • Middle Aged
  • Neoplasm Invasiveness / genetics
  • Nuclear Factor 90 Proteins / genetics*
  • Nuclear Factor 90 Proteins / metabolism*
  • PTEN Phosphohydrolase / metabolism
  • RNA, Long Noncoding / genetics*
  • RNA, Long Noncoding / metabolism*
  • Uterine Cervical Neoplasms / genetics*
  • Uterine Cervical Neoplasms / metabolism
  • Uterine Cervical Neoplasms / pathology

Substances

  • ILF3 protein, human
  • MIRN454 microRNA, human
  • MicroRNAs
  • Nuclear Factor 90 Proteins
  • RNA, Long Noncoding
  • PTEN Phosphohydrolase
  • PTEN protein, human

Grants and funding

The present study was supported by the Medical Scientific Research Foundation of Guangdong Province (grant no. B2020211), the Scientific Research Project of Guangdong Provincial Bureau of Traditional Chinese Medicine (grant no. 20201284) and the Guangzhou Health Science and Technology Project (grant no. 20202A010024).