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Ciclopirox induces autophagy through reactive oxygen species-mediated activation of JNK signaling pathway

Hongyu Zhou1, Tao Shen2, Chaowei Shang2

  • 1State Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming 650201, China. Department of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA 71130-3932, USA.

Oncotarget
|October 9, 2014
PubMed

Insights

Ciclopirox olamine (CPX) triggers autophagy in rhabdomyosarcoma cells via reactive oxygen species (ROS) and JNK signaling. Inhibiting autophagy enhances CPX

Area of Science:

  • Oncology
  • Cell Biology
  • Pharmacology

Background:

  • Ciclopirox olamine (CPX), a known fungicide, shows potential as an anticancer agent.
  • The precise anticancer mechanisms of CPX remain largely unelucidated.
  • Understanding CPX's cellular effects is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the anticancer mechanism of CPX in human rhabdomyosarcoma cells.
  • To determine the role of autophagy and related signaling pathways in CPX's effects.
  • To explore novel therapeutic strategies combining CPX with autophagy inhibitors.

Main Methods:

  • Induction of autophagy by CPX in Rh30 and RD rhabdomyosarcoma cell lines.
  • Assessment of reactive oxygen species (ROS) production using N-acetyl-L-cysteine (NAC).
  • Analysis of mitogen-activated protein kinase (MAPK) pathway activation (ERK1/2, JNK, p38).
  • Pharmacological inhibition of JNK (SP600125) and autophagy (chloroquine, CQ).

Main Results:

  • CPX treatment induced autophagy in human rhabdomyosarcoma cells.
  • CPX-induced autophagy was dependent on reactive oxygen species (ROS) generation.
  • ROS-mediated activation of the JNK signaling pathway contributed to CPX-induced autophagy.
  • Inhibition of autophagy by chloroquine (CQ) potentiated CPX-induced cell death.
  • CPX-induced autophagy plays a pro-survival role in these cancer cells.

Conclusions:

  • CPX induces autophagy in rhabdomyosarcoma cells through ROS and JNK signaling.
  • Autophagy acts as a pro-survival mechanism, limiting CPX's anticancer efficacy.
  • Combining CPX with autophagy inhibitors presents a promising strategy to enhance its therapeutic potential against rhabdomyosarcoma.

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