MiR-200c-3p increased HDMEC proliferation through the notch signaling pathway

Exp Biol Med (Maywood). 2021 Apr;246(8):897-905. doi: 10.1177/1535370220981859. Epub 2021 Jan 20.

Abstract

Excessive proliferation of vascular endothelial cells can cause hemangioma. Although typically benign, hemangiomas can become life-threatening. The microRNA miR-200c-3p is abnormally expressed in some types of tumors, but its expression, biological role, and mechanism of action in infantile hemangioma remain to be fully elucidated. The expression levels of miR-200c-3p in hemangioma tissue were compared with those in adjacent healthy tissue by using bioinformatics analyses and TargetScan. Western blot, enzyme-linked immunosorbent assay, and Cell Counting Kit 8 analyses were used to determine the biological function and site of action of miR-200c-3p in human dermal microvascular endothelial cells (HDMECs). MiR-200c-3p was one of the top 10 differentially expressed genes between healthy tissue, and hemangiomas tissues, having markedly decreased expression in hemangioma tissue. Reduction of miR-200c-3p expression in HDMECs through the transfection of a miR-200c-3p inhibitor significantly increased HDMEC proliferation. The addition of the Notch signaling pathway inhibitor DAPT to HDMECs transfected with the miR-200c-3p inhibitor eliminated the inhibitor-induced enhancement of proliferation in HDMECs. These findings indicate that miR-200c-3p targets the Notch signaling pathway to promote the proliferation of vascular endothelial cells, suggesting that miR-200c-3p plays an important role in the pathogenesis of hemangioma.

Keywords: Infantile hemangioma; cell proliferation; miR-200c-3p; notch signaling pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Proliferation*
  • Dermis / blood supply
  • Dermis / metabolism*
  • Endothelial Cells / metabolism*
  • Gene Expression Regulation
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Microvessels / metabolism*
  • Receptors, Notch / genetics
  • Receptors, Notch / metabolism*
  • Signal Transduction*

Substances

  • MIRN200 microRNA, human
  • MicroRNAs
  • Receptors, Notch