Quercetin and sorafenib as a novel and effective couple in programmed cell death induction in human gliomas

Joanna Jakubowicz-Gil1, Ewa Langner, Dorota Bądziul

  • 1Department of Comparative Anatomy and Anthropology, Maria Curie-Skłodowska University, Akademicka 19, 20-033, Lublin, Poland, jjgil@poczta.umcs.lublin.pl.

Neurotoxicity Research
|December 25, 2013
PubMed

Insights

Sorafenib and quercetin effectively induce programmed cell death in glioblastoma and anaplastic astrocytoma cells. Inhibiting heat shock proteins enhances this effect, offering a promising therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Glioblastoma multiforme (T98G) and anaplastic astrocytoma (MOGGCCM) are aggressive brain tumors.
  • Understanding cell death pathways like apoptosis and autophagy is crucial for developing new cancer therapies.

Purpose of the Study:

  • To investigate the effects of sorafenib and quercetin on apoptosis and autophagy in MOGGCCM and T98G cell lines.
  • To explore the combined effects of these drugs and the role of heat shock proteins.

Main Methods:

  • Treatment of MOGGCCM and T98G cells with sorafenib and quercetin.
  • Analysis of apoptosis via mitochondrial pathway markers (caspase 9, 3) and cytochrome c release.
  • Assessment of autophagy through beclin 1 and LC3II expression.
  • Utilizing small interfering RNA to inhibit heat shock proteins.

Main Results:

  • Sorafenib induced apoptosis in MOGGCCM cells and autophagy in T98G cells.
  • Quercetin potentiated sorafenib's pro-apoptotic effects and increased autophagy when administered sequentially.
  • Simultaneous drug application favored apoptosis over autophagy.
  • Inhibition of heat shock proteins significantly enhanced apoptosis induction in both cell lines.

Conclusions:

  • Sorafenib and quercetin are potent inducers of programmed cell death in MOGGCCM and T98G cells.
  • Combined treatment, especially with heat shock protein inhibition, shows significant potential for glioblastoma therapy.

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