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MicroRNA-133a downregulated EGFR expression in human non-small cell lung cancer cells via AKT/ERK signaling

Nannan Guo1, Yingnan Zhao1, Wen Zhang1

  • 1Department of Cardiothoracic Surgery, The First Affiliated Hospital of General Hospital of The Chinese People's Liberation Army, Beijing 100048, P.R. China.

Oncology Letters
|October 19, 2018
PubMed

Insights

MicroRNA-133a (miRNA-133a) suppresses non-small cell lung cancer (NSCLC) growth by downregulating epidermal growth factor receptor (EGFR) and inhibiting the AKT/ERK pathway. This study reveals miRNA-133a as a potential therapeutic target for NSCLC.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • MicroRNAs (miRNAs) are implicated in regulating non-small cell lung cancer (NSCLC) cell growth and apoptosis.
  • The specific role of miRNA-133a in NSCLC, particularly its interaction with the epidermal growth factor receptor (EGFR) and the AKT/extracellular signal-regulated kinase (ERK) pathway, remains largely unexplored.

Purpose of the Study:

  • To investigate the role of miRNA-133a in regulating NSCLC cell growth and apoptosis.
  • To elucidate the molecular mechanism involving the epidermal growth factor receptor (EGFR) and the AKT/extracellular signal-regulated kinase (ERK) signaling pathway.

Main Methods:

  • Comparative analysis of miRNA-133a and EGFR expression levels in NSCLC tissues versus adjacent mucosa.
  • Experimental manipulation of miRNA-133a expression in NSCLC cells.
  • Assessment of cell growth, apoptosis, and protein expression (caspase-3, EGFR, p-AKT, p-ERK).

Main Results:

  • Lower miRNA-133a and higher EGFR expression were observed in NSCLC tissues.
  • Upregulation of miRNA-133a suppressed NSCLC cell growth and induced apoptosis.
  • Increased miRNA-133a led to elevated caspase-3 and reduced EGFR, p-AKT, and p-ERK protein levels.

Conclusions:

  • MiRNA-133a acts as a tumor suppressor in NSCLC by downregulating EGFR expression.
  • The mechanism involves the inhibition of the AKT/ERK signaling pathway.
  • MiRNA-133a represents a potential therapeutic target for NSCLC treatment.
Keywords:
AKTepidermal growth factor receptorextracellular signal-regulated kinasemicroRNA-133anon-small cell lung cancer

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