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Induction and Analysis of Epithelial to Mesenchymal Transition
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Association of cell cycle arrest with anticancer drug-induced epithelial-mesenchymal transition in alveolar

Masashi Kawami1, Risako Harada1, Takamichi Ojima1

  • 1Department of Pharmaceutics and Therapeutics, Graduate School of Biomedical & Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.

Toxicology
|June 7, 2019
PubMed

Insights

Anticancer drugs can cause lung injury by inducing epithelial-mesenchymal transition (EMT). This study reveals that cell cycle arrest, particularly at S- and G2/M-phases, is closely linked to MTX- and PTX-induced EMT in lung cells.

Area of Science:

  • Pulmonary Pharmacology
  • Cell Biology
  • Drug Toxicology

Background:

  • Anticancer drugs can cause significant lung tissue damage.
  • Epithelial-mesenchymal transition (EMT) is implicated in drug-induced lung injury, but mechanisms remain unclear.

Purpose of the Study:

  • To investigate the mechanisms underlying anticancer drug-induced EMT.
  • To determine the role of cell cycle arrest in this process.

Main Methods:

  • Microarray analysis to assess gene expression changes induced by methotrexate (MTX).
  • Gene set enrichment analysis to identify associated pathways.
  • Treatment with thymidine (THY) and nocodazole (NOC) to induce cell cycle arrest.
  • Assessment of alpha-smooth muscle actin (α-SMA) expression at mRNA and protein levels.

Main Results:

  • MTX altered mRNA expression, with cell cycle arrest pathways linked to EMT.
  • THY and NOC increased α-SMA mRNA levels, indicating EMT.
  • α-SMA protein levels were higher in cells arrested at S- and G2/M-phases by MTX and paclitaxel (PTX).
  • Combined treatment with cell cycle arrest agents and EMT-inducing drugs did not further increase α-SMA mRNA.

Conclusions:

  • Cell cycle arrest, specifically at S- and G2/M-phases, is closely associated with anticancer drug-induced EMT in alveolar epithelial cells.
  • This suggests cell cycle modulation as a potential factor in drug-induced lung injury.
Keywords:
Alveolar epithelial cellsAnticancer drugsCell cycle arrestEpithelial-mesenchymal transitionMicroarray

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