MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1

Hongwei Yang*, Yonggang Huang, Jian He, Guangrui Chai, Yu Di, Aiyuan Wang, Dongmei Gui

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

It has been reported that miR-486-3p expression is decreased in retinoblastoma (RB) tumor tissues, however, its function in RB has been less reported. The present study aimed to explore the regulatory effects of miR-486-3p on RB cells. The expression of miR-486-3p in RB tissues and cells was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, proliferation, apoptosis, migration and invasion ability were determined by cell counting kit-8 (CCK-8) kit, clone formation assay, flow cytometry, scratch assay and transwell, respectively. Targetscan 7.2 and dual-luciferase reporter were used to verify target genes for miR-486-3p. The expressions of apoptosis-related proteins and ECM1 were detected by Western blot. The miR-486-3p expression was decreased in RB tissues and cells. In RB cells, overexpression of miR-486-3p inhibited cell proliferation, migration and invasion, while promoted apoptosis. Moreover, overexpression of miR-486-3p decreased Bcl-2 expression, while increased the expressions of Bax and Cleaved Caspase-3 (C caspase-3). ECM1 was the target gene of miR-486-3p, and miR-486-3p inhibited the expression of ECM1. Furthermore, ECM1 partially reversed the inhibitory effect of miR-486-3p on the proliferation, migration and invasion of RB cells. MiR-486-3p inhibited the proliferation, migration and invasion of RB by down-regulating ECM1.

Original languageEnglish (US)
Article numberBSR20200392
JournalBioscience Reports
Volume40
Issue number6
DOIs
StatePublished - Jun 2020

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'MiR-486-3p inhibits the proliferation, migration and invasion of retinoblastoma cells by targeting ECM1'. Together they form a unique fingerprint.

  • Cite this