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GdCl3 induced Hep G2 cell death through mitochondrial and external death pathways without significant elevation of

Lihua Ye1, Zhe Shi, Huixue Liu

  • 1State Key Laboratories of Natural and Biomimetic Drugs, Peking University, Beijing, People's Republic of China.

Biological Trace Element Research
|November 7, 2012
PubMed

Insights

Gadolinium chloride (GdCl3) induces programmed cell death (apoptosis) in hepatoblastoma cells via intrinsic and external pathways. This anticancer mechanism occurs without significant oxidative stress, offering new insights for developing gadolinium-based anticancer agents.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Gadolinium (Gd) compounds are utilized as MRI contrast agents.
  • Gd compounds show potential as anticancer agents.
  • Hepatoblastoma is a rare malignant tumor affecting the liver.

Purpose of the Study:

  • To investigate the proapoptotic mechanisms of gadolinium chloride (GdCl3) in hepatoblastoma (Hep G2) cells.
  • To elucidate the role of oxidative stress in GdCl3-induced apoptosis.
  • To explore the signaling pathways involved in GdCl3-mediated cell death.

Main Methods:

  • Treatment of Hep G2 cells with GdCl3 at varying concentrations and incubation times.
  • Assessment of apoptosis through markers like cytochrome c (Cyt c) release, caspase activation, and mitochondrial membrane potential.
  • Analysis of signaling pathways including extracellular signal-regulated kinase (ERK) and c-Jun NH2 terminal kinase (JNK) activation.
  • Evaluation of oxidative stress levels.

Main Results:

  • GdCl3 induced apoptosis in Hep G2 cells at high concentrations and prolonged incubation.
  • Apoptosis involved intrinsic and extrinsic pathways: Cyt c and apoptosis-inducing factor release, Bax translocation, mitochondrial dysfunction, caspase 3 and 8 activation, and Bid cleavage.
  • GdCl3 did not induce significant oxidative stress in tumor cells.
  • Activation of ERK and JNK pathways was observed and inhibition of these kinases attenuated GdCl3-induced apoptosis.

Conclusions:

  • GdCl3 triggers apoptosis in hepatoblastoma cells through both intrinsic and extrinsic pathways.
  • The anticancer effect of GdCl3 on Hep G2 cells occurs independently of significant reactive oxygen species generation.
  • These findings provide novel insights into the biological effects of GdCl3 and its potential as an anticancer therapeutic agent.

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