LINC01116 promotes proliferation and migration of endometrial stromal cells by targeting FOXP1 via sponging miR-9-5p in endometriosis

J Cell Mol Med. 2021 Feb;25(4):2000-2012. doi: 10.1111/jcmm.16039. Epub 2020 Dec 28.

Abstract

Endometriosis is a common multi-factorial gynaecological disease. Recent studies have revealed that long non-coding RNAs (lncRNAs) are involved in the pathogenesis of endometriosis. In the present study, the expression profiles of lncRNAs in 6 pairs of endometriosis ectopic endometrium (ecEM) and eutopic endometrium (euEM) tissues were analysed by RNA sequencing. From the profiles, LINC01116 was found to be up-regulated in ecEM tissues compared to euEM tissues and was verified by quantitative real-time PCR (qRT-PCR). Then, functional experiments demonstrated that LINC01116 promoted the proliferation and migration of ectopic primary endometrial stromal cells (ESCs), while miR-9-5p exerted the opposite effects. Dual-luciferase reporter assays verified that LINC01116 directly sponged miR-9-5p and relieved the suppression of its target, Forkhead box protein P1 (FOXP1). Rescue experiments further demonstrated that LINC01116 could promote proliferation and migration of ESCs by targeting FOXP1 via sponging miR-9-5p. Overall, our study illuminates that LINC01116 promotes the progression of endometriosis through the miR-9-5p/FOXP1 axis. This finding provides a novel therapeutic target for patients with endometriosis.

Keywords: FOXP1; LINC01116; ceRNA; endometriosis; miR-9-5p.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cell Movement
  • Cell Proliferation
  • Computational Biology / methods
  • Disease Susceptibility
  • Endometriosis / genetics*
  • Endometriosis / metabolism
  • Female
  • Forkhead Transcription Factors / genetics*
  • Gene Expression Profiling
  • Gene Expression Regulation*
  • High-Throughput Nucleotide Sequencing
  • Humans
  • MicroRNAs / genetics*
  • RNA Interference*
  • Repressor Proteins / genetics*
  • Stromal Cells / metabolism*
  • Transcriptome
  • Young Adult

Substances

  • FOXP1 protein, human
  • Forkhead Transcription Factors
  • MIRN92 microRNA, human
  • MicroRNAs
  • Repressor Proteins