Expression and mechanism of microRNA-181A on incidence and survival in late liver metastases of colorectal cancer

Oncol Rep. 2016 Mar;35(3):1403-8. doi: 10.3892/or.2016.4546. Epub 2016 Jan 5.

Abstract

The emerging role of microRNA-181A (miR-181A) in CRC patients with late liver metastases was studied. In the present study we investigated the association between expression and mechanism of miRNA-181A, liver metastasis and prognosis of colorectal cancer (CRC). The expression of miR-181A and PTEN in CRC patients with late liver metastases was higher than that of the normal (control) group, whereas the expression of miR-181A and PTEN was lower in all pathological groups (TNM I-TNM IV). Overall survival (OS) of lower expression miR-181A CRC patients with late liver metastases was higher than that of higher expression miR-181A CRC patients with late liver metastases. The expression of miR-181A and PTEN in the colon cell line NCM460 was lower than that of the colon cancer SW620 cell line. Upregulation of miR-181A promoted cell viability and inhibited apoptosis of SW620 cells, suppressed PTEN expression and activated phosphorylation of AKT (p-AKT) in SW620 cells. Additionally, downregulation of miR-181A inhibited cell viability of SW620 cells through promotion of PTEN and inhibition of p-AKT. Together, our results indicate that miR-181A expression is associated with CRC patients with late liver metastases through PTEN/AKT signaling.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis
  • Cell Proliferation / genetics
  • Colorectal Neoplasms / genetics*
  • Colorectal Neoplasms / pathology
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Kaplan-Meier Estimate
  • Liver Neoplasms / genetics*
  • Liver Neoplasms / pathology
  • Liver Neoplasms / secondary
  • Male
  • MicroRNAs / biosynthesis*
  • MicroRNAs / genetics
  • Neoplasm Metastasis
  • PTEN Phosphohydrolase / biosynthesis
  • PTEN Phosphohydrolase / genetics*
  • Prognosis
  • Proto-Oncogene Proteins c-akt / biosynthesis
  • Proto-Oncogene Proteins c-akt / genetics*
  • Signal Transduction

Substances

  • MIrn181 microRNA, human
  • MicroRNAs
  • Proto-Oncogene Proteins c-akt
  • PTEN Phosphohydrolase
  • PTEN protein, human