MicroRNA‑500a‑5p inhibits colorectal cancer cell invasion and epithelial‑mesenchymal transition

Int J Oncol. 2020 Jun;56(6):1499-1508. doi: 10.3892/ijo.2020.5015. Epub 2020 Mar 19.

Abstract

The development of malignant tumors is a series of complex processes, the majority of which have not been elucidated. The aim of the present study was to investigate the microRNAs (miRNAs/miR) that affect the migration and invasion abilities of CRC cells. Our previous reports have revealed that miR‑500a‑5p suppressed CRC cell growth and malignant transformation. The present study demonstrated that overexpression of miR‑500a‑5p reduced the expression of vimentin, while increasing the expression of E‑cadherin. Inhibition of miR‑500a‑5p resulted in spindle‑like morphological changes and reorganization of F‑actin in CRC cells. Furthermore, miR‑500a‑5p attenuated the transforming growth factor‑β signaling pathway in EMT. Additionally, emodin inhibited the miR‑500a‑5p inhibitor and suppressed the EMT process. In animal models of metastasis using nude mice, EMT and LoVo cell metastasis was modulated by miR‑500a‑5p. Therefore, the findings of the present study demonstrated that miR‑500a‑5p is associated with a positive therapeutic outcome in terms of invasion/migration of CRC cells and mesenchymal‑like cell changes.

Keywords: miR-500a-5p; epithelial-mesenchymal transition; transforming growth factor-β1; colorectal cancer; emodin.

MeSH terms

  • Actins / genetics
  • Actins / metabolism
  • Animals
  • Antigens, CD / genetics
  • Antigens, CD / metabolism
  • Cadherins / genetics
  • Cadherins / metabolism
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Cell Survival
  • Colorectal Neoplasms / genetics
  • Colorectal Neoplasms / pathology*
  • Down-Regulation*
  • Epithelial-Mesenchymal Transition
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Mice
  • Mice, Nude
  • MicroRNAs / genetics*
  • Neoplasm Invasiveness
  • Neoplasm Transplantation
  • Signal Transduction*
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / metabolism
  • Vimentin / genetics
  • Vimentin / metabolism

Substances

  • Actins
  • Antigens, CD
  • CDH1 protein, human
  • Cadherins
  • MicroRNAs
  • TGFB1 protein, human
  • Transforming Growth Factor beta1
  • VIM protein, human
  • Vimentin