miR-646 is a key negative regulator of EGFR pathway in lung cancer

Exp Lung Res. 2016 Aug;42(6):286-95. doi: 10.1080/01902148.2016.1207726. Epub 2016 Jul 27.

Abstract

Background: As one of the leading cause of cancer-related deaths in the worldwide, lung cancer needs to be understood better. Nowadays, increasing point mutations of specific oncogenes are biomarkers used to predict the therapeutic effect of targeted therapy and lung cancer has entered the age of individual treatment. At present, many relevant researchers have suggested that EGFR is a biomarker used to predict the therapeutic effect of targeted therapy. A large number of evidence indicates that EGFR/Akt pathway plays important role in cancer growth and metastasis.

Aim of the study: In this paper, we found EGFR was a target of miR-646.

Results: Overexpression of miR-646 not only downregulated EGFR/Akt pathway, but also inhibited lung cancer cell proliferation and metastasis. At the same time, miR-646 was a prognosis factor for overall survival.

Conclusion: Our finding could provide new insights into the molecular therapeutic of lung cancer.

Keywords: EGFR; lung cancer; metastasis; prognosis; proliferation.

MeSH terms

  • A549 Cells
  • Adult
  • Aged
  • Animals
  • Antagomirs / pharmacology
  • Antagomirs / therapeutic use*
  • Drug Evaluation, Preclinical
  • ErbB Receptors / metabolism*
  • Humans
  • Lung Neoplasms / metabolism*
  • Male
  • Mice, Inbred BALB C
  • Mice, Nude
  • MicroRNAs / antagonists & inhibitors
  • MicroRNAs / metabolism*
  • Middle Aged
  • Molecular Targeted Therapy
  • Neoplasm Transplantation
  • Proto-Oncogene Proteins c-akt / metabolism
  • Random Allocation

Substances

  • Antagomirs
  • MIRN646 microRNA, human
  • MIRN646 microRNA, mouse
  • MicroRNAs
  • EGFR protein, human
  • ErbB Receptors
  • Proto-Oncogene Proteins c-akt