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TMEPAI regulates EMT in lung cancer cells by modulating the ROS and IRS-1 signaling pathways

Ying Hu1, Kai He, Dongmei Wang

  • 1State Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, PR China.

Carcinogenesis
|April 26, 2013
PubMed

Insights

Prostate transmembrane protein, androgen induced-1 (TMEPAI) drives lung cancer progression by promoting epithelial-mesenchymal transition (EMT). TMEPAI facilitates EMT via reactive oxygen species (ROS) and insulin receptor substrate-1 (IRS-1) signaling, highlighting its role in metastasis.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Epithelial-mesenchymal transition (EMT) is crucial for cancer cell migration and metastasis.
  • Reactive oxygen species (ROS) and insulin receptor substrate-1 (IRS-1) are key regulators in cancer progression and EMT.
  • The role of prostate transmembrane protein, androgen induced-1 (TMEPAI) in EMT and lung cancer requires further elucidation.

Purpose of the Study:

  • To investigate the expression, function, and signaling pathway of TMEPAI during EMT induction and cell migration in human lung adenocarcinoma.
  • To determine the regulatory mechanism of TMEPAI in TGF-β1-induced EMT and its correlation with cancer progression.

Main Methods:

  • Quantitative analysis of TMEPAI expression in lung adenocarcinoma cells and tissues.
  • Manipulation of TMEPAI levels using depletion and overexpression techniques.
  • Assessment of ROS generation, ferritin heavy chain, and IRS-1 levels.
  • Evaluation of TGF-β1-induced EMT and cell migration assays.
  • In vivo correlation of TMEPAI expression with tumor characteristics.

Main Results:

  • Transforming growth factor (TGF)-β1 significantly upregulated TMEPAI expression during EMT in lung adenocarcinoma.
  • TMEPAI depletion abolished TGF-β1-induced downregulation of ferritin heavy chain and ROS generation, suppressing EMT and migration.
  • Increased ROS and TMEPAI overexpression led to IRS-1 downregulation.
  • TMEPAI levels were significantly elevated in lung tumor tissues compared to normal epithelium and correlated positively with mesenchymal phenotype and migration potential.

Conclusions:

  • TMEPAI is a critical mediator of TGF-β1-induced EMT in lung cancer.
  • TMEPAI promotes EMT by increasing ROS production and downregulating IRS-1.
  • TMEPAI expression is a potential biomarker for lung cancer progression and metastasis.

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