MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2

Bioengineered. 2021 Dec;12(1):4044-4053. doi: 10.1080/21655979.2021.1951930.

Abstract

A large number of studies have shown that microRNA (miRNA) has an important relationship with the occurrence and development of colorectal cancer (CRC), but its specific molecular mechanism has not been fully elucidated. This study is to explore the influence of miR-506-3p on the malignant behavior of CRC and its underlying molecular mechanism. Our results show that miR-506-3p was lowly expressed and enhancer of zeste homologue 2 (EZH2) was highly expressed in CRC. Overexpressing miR-506-3p or silencing EZH2 inhibited CRC cell proliferation, migration and invasion and promoted apoptosis. Inhibiting miR-506-3p promoted CRC cell proliferation, migration and invasion but inhibited apoptosis. These impacts were reversed after co-transfecting si-EZH2. Further mechanism studies have shown that miR-506-3p can reduce EZH2 expression in CRC cells by binding to the 3'UTR end of EZH2. In summary, the results of this study show that miR-506-3p inhibited CRC progression through targeting EZH2 expression. This provides a new molecular target for the clinical treatment of CRC in the future.

Keywords: Mir-506-3p; colorectal cancer; enhancer of zeste homologue 2 (ezh2).

MeSH terms

  • Base Sequence
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / pathology*
  • Disease Progression
  • Down-Regulation / genetics
  • Enhancer of Zeste Homolog 2 Protein / genetics
  • Enhancer of Zeste Homolog 2 Protein / metabolism*
  • Gene Expression Regulation, Neoplastic
  • Gene Silencing
  • Humans
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Up-Regulation / genetics

Substances

  • MIRN506 microRNA, human
  • MicroRNAs
  • EZH2 protein, human
  • Enhancer of Zeste Homolog 2 Protein

Grants and funding

The authors have no funding to report.