PUBLICATION

miR-608 regulates apoptosis in human lung adenocarcinoma via regulation of AKT2

Authors
Othman, N., Nagoor, N.H.
ID
ZDB-PUB-171028-7
Date
2017
Source
International Journal of Oncology   51(6): 1757-1764 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • 3' Untranslated Regions
  • A549 Cells
  • Adenocarcinoma/enzymology*
  • Adenocarcinoma/genetics*
  • Animals
  • Apoptosis/physiology
  • Caspase 3/metabolism
  • Gene Silencing
  • Heterografts
  • Humans
  • Lung Neoplasms/enzymology*
  • Lung Neoplasms/genetics*
  • MicroRNAs/genetics*
  • MicroRNAs/metabolism*
  • Proto-Oncogene Proteins c-akt/genetics*
  • Proto-Oncogene Proteins c-akt/metabolism
  • Transfection
  • Zebrafish
PubMed
29075783 Full text @ Int. J. Oncol.
Abstract
Lung cancer remains a major health problem with a low 5-year survival rate of patients. Recent studies have shown that dysregulation of microRNAs (miRNAs) are prevalent in lung cancer and these aberrations play a significant role in the progression of tumour progression. In the present study, bioinformatics analyses was employed to predict potential miR-608 targets, which are associated with signaling pathways involved in cancer. Luciferase reporter assay identified AKT2 as a novel target of miR-608, and suppression of its protein levels was validated through western blot analysis. Zebrafish embryos were microinjected with cells transfected with miR-608 to elucidate the role of miR-608 in vivo, and immunostained with antibodies to detect activated caspase-3. We present the first evidence that miR-608 behaves as a tumour suppressor in A549 and SK-LU-1 cells through the regulation of AKT2, suggesting that selective targeting of AKT2 via miR-608 may be developed as a potential therapeutic strategy for miRNA-based non-small cell lung cancer (NSCLC) therapy.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping