LINC00528 regulates myocardial infarction by targeting the miR-143-3p/COX-2 axis

Bioengineered. 2020 Dec;11(1):11-18. doi: 10.1080/21655979.2019.1704535.


This study is aimed to explore the roles of LINC00528 in myocardial infarction (MI) progression. Quantitative real-time PCR showed that the expression of LINC00528 and COX-2 was upregulated while miR-143-3p expression was down-regulated in post-MI cells. In function assays, LINC00528 suppression promoted post-MI cells proliferation and reduced cell apoptosis in vitro. In mechanism, LINC00528 interacted with miR-143-3p in post-MI cells. COX-2 served as a target of miR-143-3p in post-MI cells. Besides, LINC00528 inhibition on COX-2 expression and post-MI cells progression could be partially abolished by miR-143-3p inhibitors. Therefore, our findings suggested that LINC00528 exerted its regulatory roles in MI via the miR-143-3p/COX-2 axis, which provided a potential therapeutic target for MI patients treatment.

Keywords: COX-2; LINC00528; Myocardial infarction; miR-143-3p.

MeSH terms

  • Apoptosis
  • Cell Line
  • Cell Proliferation
  • Cyclooxygenase 2 / genetics*
  • Cyclooxygenase 2 / metabolism
  • Down-Regulation
  • Gene Expression Regulation
  • Humans
  • MicroRNAs / genetics*
  • MicroRNAs / metabolism
  • Myocardial Infarction / genetics*
  • Myocardial Infarction / metabolism
  • Myocardial Infarction / physiopathology
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism*


  • MIRN143 microRNA, human
  • MicroRNAs
  • RNA, Long Noncoding
  • Cyclooxygenase 2