[α-Enolase (ENO1) inhibits epithelial-mesenchymal transition in the A549 cell line
by suppressing ERK1/2

Related Experiment Video

Updated: May 11, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

Xin Zhou1, Ying Zhang, Naijun Han

  • 1State Key Laboratory of Molecular Oncology, Beijing Key Laboratory of Carcinogenesis and Cancer Prevention, Cancer Institute, Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.

Zhongguo Fei AI Za Zhi = Chinese Journal of Lung Cancer
|May 17, 2013
PubMed
Abstract

Insights

Overexpressing ENO1 in non-small cell lung cancer (NSCLC) cells inhibits epithelial-mesenchymal transition (EMT) by reducing ERK1/2 phosphorylation. This finding offers potential therapeutic targets for NSCLC metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Context:

  • Epithelial-mesenchymal transition (EMT) is crucial for non-small cell lung cancer (NSCLC) progression and metastasis.
  • Canonical MAPK signaling pathways, particularly those involving transforming growth factor β (TGFβ), regulate EMT.
  • Understanding the molecular mechanisms underlying EMT in NSCLC is vital for developing targeted therapies.

Purpose:

  • To investigate the role of ENO1 in regulating EMT in the A549 NSCLC cell line.
  • To elucidate the molecular mechanism by which ENO1 affects EMT, focusing on its interaction with signaling pathways.

Summary:

  • ENO1 overexpression in A549 cells significantly inhibited cell mobility and suppressed key mesenchymal markers (N-cadherin, vimentin) while upregulating the epithelial marker (E-cadherin).
  • Further assays confirmed that ENO1 negatively impacts EMT, even under TGFβ-1 induction.
  • ENO1 overexpression was found to suppress ERK1/2 phosphorylation in response to EGF stimulation, indicating a role in MAPK signaling inhibition.

Impact:

  • ENO1 acts as an inhibitor of EMT in NSCLC cells.
  • Overexpression of ENO1 suppresses EMT by inhibiting ERK1/2 phosphorylation, suggesting a potential therapeutic strategy for NSCLC.
  • This research provides insights into the molecular regulation of EMT in NSCLC, potentially leading to novel treatment approaches.

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