MicroRNA-10b Triggers the Epithelial-Mesenchymal Transition (EMT) of Laryngeal Carcinoma Hep-2 Cells by Directly Targeting the E-cadherin

Appl Biochem Biotechnol. 2015 May;176(1):33-44. doi: 10.1007/s12010-015-1505-6. Epub 2015 Feb 10.

Abstract

Laryngeal carcinoma is the second most common malignancy of the head and neck squamous cell carcinoma. Therefore, there is an urgent need to understand the molecular mechanism of its metastasis. The present study was designed to investigate effects of miR-10b on the invasion and migration of laryngeal Hep-2 cells. We found that miR-10b had limited effects on cell proliferation; however, it can significantly promote the migration and invasion of Hep-2 cells. Further studies revealed that overexpression of miR-10b can induce the epithelial-mesenchymal transition (EMT) of Hep-2 cells by acquiring mesenchymal spindle-like morphology and increasing the expression of N-cadherin (N-Cad) with a concomitant decrease of E-cadherin (E-Cad). However, the messenger RNA (mRNA) and protein level of transcription factors such as Snail, Slug, Twist and ZEB was not changed during this process. Bioinformatic analysis revealed that miR-10b can directly target CDH1 (E-Cad gene) at nucleotides 461 and 481 within the 3'-UTR. This was confirmed by the results that miR-10 downregulated the protein and mRNA levels of E-Cad via a time-dependent manner and luciferase analysis by use of four-nucleotide substitution in the core binding sites. The present study provided a better understanding of laryngeal carcinoma metastasis and the roles of miR-10b during this process.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, CD
  • Cadherins / genetics
  • Cadherins / metabolism*
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Epithelial-Mesenchymal Transition*
  • Humans
  • Laryngeal Neoplasms / genetics
  • Laryngeal Neoplasms / metabolism*
  • Laryngeal Neoplasms / pathology
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*
  • RNA, Neoplasm / genetics
  • RNA, Neoplasm / metabolism*

Substances

  • Antigens, CD
  • CDH1 protein, human
  • Cadherins
  • MIRN10 microRNA, human
  • MicroRNAs
  • Neoplasm Proteins
  • RNA, Neoplasm