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Cytotoxic effects of 15d-PGJ2 against osteosarcoma through ROS-mediated AKT and cell cycle inhibition

Chueh-Chuan Yen1, Chung-Der Hsiao, Wei-Ming Chen

  • 1Division of Hematology and Oncology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.

Oncotarget
|February 26, 2014
PubMed

Insights

15-deoxy-Δ12, 14-prostaglandin J2 (15d-PGJ2) shows anti-cancer effects against osteosarcoma (OS) by inducing apoptosis. This involves down-regulating AKT and PKA-PLK1 pathways via reactive oxygen species (ROS) and JNK activation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Polo-like kinase 1 (PLK1) is a key cell cycle regulator and potential osteosarcoma (OS) target.
  • 15-deoxy-Δ12, 14-prostaglandin J2 (15d-PGJ2) exhibits anti-tumor activity by inducing apoptosis via ROS-mediated AKT inactivation.
  • 15d-PGJ2 has been shown to induce chondrocyte apoptosis through PKA-dependent regulation of PLK1.

Purpose of the Study:

  • To investigate the cytotoxic effects and underlying mechanisms of 15d-PGJ2 against OS cell lines.
  • To explore the role of AKT and PKA-PLK1 pathways in 15d-PGJ2-induced OS cell death.
  • To determine the involvement of reactive oxygen species (ROS) and JNK signaling in 15d-PGJ2's anti-cancer activity.

Main Methods:

  • Treatment of OS cell lines with 15d-PGJ2.
  • Cell cycle analysis (G2/M arrest).
  • Western blot analysis for AKT, PKA-PLK1, and phosphorylated proteins.
  • ROS generation assays and rescue experiments with N-acetyl-l-cysteine.
  • Rescue experiments with constitutively active AKT or PLK1.
  • JNK inhibition experiments.

Main Results:

  • 15d-PGJ2 induced significant G2/M arrest and exhibited time- and dose-dependent cytotoxicity in OS cells.
  • Western blot analysis revealed down-regulation of AKT and PKA-PLK1 following 15d-PGJ2 treatment.
  • Overexpression of active AKT or PLK1 partially rescued cells from 15d-PGJ2-induced apoptosis.
  • 15d-PGJ2 treatment increased ROS generation, and its cytotoxic effect was reversed by N-acetyl-l-cysteine.
  • Inhibition of JNK partially rescued 15d-PGJ2-induced cytotoxicity.
  • ROS-mediated JNK activation contributes to apoptosis via down-regulation of p-Akt and PKA-PLK1.

Conclusions:

  • 15d-PGJ2 demonstrates significant cytotoxic effects against osteosarcoma cells.
  • The anti-cancer mechanism involves ROS-mediated JNK activation, leading to the down-regulation of AKT and PKA-PLK1 pathways.
  • 15d-PGJ2 is a potential therapeutic agent for OS, warranting further investigation in preclinical and clinical studies.

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