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The ROS/JNK/ATF2 pathway mediates selenite-induced leukemia NB4 cell cycle arrest and apoptosis in vitro and in vivo

J J An1, K J Shi1, W Wei1

  • 1State Key Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences and School of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.

Cell Death & Disease
|December 21, 2013
PubMed

Insights

Selenium compounds (selenite) show antitumor potential by halting cancer cell growth. This study reveals selenite induces cell cycle arrest and apoptosis in NB4 cells via reactive oxygen species (ROS) and the JNK/ATF2 pathway.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Selenite exhibits antitumor properties, but its underlying mechanisms remain unclear.
  • Previous research suggests selenite can inhibit cancer cell proliferation.

Purpose of the Study:

  • To elucidate the mechanism by which selenite inhibits cancer cell growth, focusing on NB4 cells.
  • To investigate the role of the JNK/ATF2 axis and reactive oxygen species (ROS) in selenite's antitumor effects.

Main Methods:

  • Cell cycle analysis and apoptosis assays were performed on NB4 cells treated with selenite.
  • Western blotting was used to assess the JNK/ATF2 signaling pathway.
  • In vitro and in vivo experiments were conducted to validate findings.

Main Results:

  • Selenite induced cell cycle arrest at the G0/G1 phase and apoptosis in NB4 cells.
  • Selenite treatment inhibited the JNK/ATF2 signaling pathway.
  • Selenite-induced reactive oxygen species (ROS) were identified as upstream regulators of the JNK/ATF2 axis, cell cycle arrest, and apoptosis.
  • Inactivation of ATF2 reduced the expression of cyclin A, cyclin D3, and CDK4, contributing to G0/G1 arrest.
  • In vivo studies confirmed selenite's antitumor activity and the proposed mechanisms.

Conclusions:

  • Selenite-induced ROS trigger G0/G1 cell cycle arrest in NB4 cells by inhibiting the JNK/ATF2 pathway.
  • These findings provide a mechanistic understanding of selenite's antitumor effects in vitro and in vivo.

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