The long noncoding RNA MALAT-1 functions as a competing endogenous RNA to regulate MSL2 expression by sponging miR-338-3p in myasthenia gravis

J Cell Biochem. 2019 Apr;120(4):5542-5550. doi: 10.1002/jcb.27838. Epub 2018 Oct 26.

Abstract

Myasthenia gravis (MG) is a cell-dependent autoimmune disease commonly associated with thymic pathology. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) has been associated with gene regulation and alternative splicing. It has shown relationship with proliferation, apoptosis, migration, and invasion. In this study, we found that MALAT-1 expression was downregulated in MG. The level of the miR-338-3p was increased in peripheral blood mononuclear cells from MG patients compared with those from control subjects. MALAT-1 competed for binding to miR-338-3p with male-specific lethal 2 (MSL2) in luciferase reporter assays. We confirmed the MALAT-1-miR-338-3p-MSL2 interaction network in MG in vitro. Thus, MALAT-1 directly induced MSL2 expression in MG by acting as a competing endogenous RNA for miR-338-3p, suggesting that it may serve as a therapeutic target for MG treatment.

Keywords: cell; competing endogenous RNA (ceRNA); immune disease; metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1); myasthenia gravis (MG).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Female
  • Gene Expression Regulation, Enzymologic*
  • Humans
  • Male
  • MicroRNAs / biosynthesis*
  • Middle Aged
  • Myasthenia Gravis / metabolism*
  • Myasthenia Gravis / pathology
  • Neoplasm Proteins / biosynthesis*
  • RNA, Long Noncoding / biosynthesis*
  • RNA, Neoplasm / biosynthesis*
  • Ubiquitin-Protein Ligases / biosynthesis*

Substances

  • MALAT1 long non-coding RNA, human
  • MIRN338 microRNA, human
  • MicroRNAs
  • Neoplasm Proteins
  • RNA, Long Noncoding
  • RNA, Neoplasm
  • MSL2 protein, human
  • Ubiquitin-Protein Ligases