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The FGFR Inhibitor NVP-BGJ398 Induces NSCLC Cell Death by Activating Caspase-dependent Pathways as well as

Antonia Göke1, Rüdiger Göke2, Andrea Ofner3

  • 1Research Unit of Gastroenterology, Center for Tumor and Immunobiology, Faculty of Medicine, University of Marburg, Marburg, Germany.

Anticancer Research
|October 28, 2015
PubMed
Abstract

Insights

NVP-BGJ398 triggers cancer cell death in non-small cell lung cancer (NSCLC) by activating apoptosis and cell cycle arrest. This study highlights small Fibroblast Growth Factor Receptor (FGFR) inhibitors as a potential cancer therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Fibroblast growth factor receptors (FGFRs) are crucial in tumor development.
  • FGFR activation drives tumor progression via cell-cycle, angiogenesis, and survival pathways.

Purpose of the Study:

  • To investigate the effects of NVP-BGJ398 on non-small cell lung cancer (NSCLC) cell line H1581.
  • To elucidate the mechanisms of NVP-BGJ398-induced growth inhibition.

Main Methods:

  • Treatment of NSCLC H1581 cells with NVP-BGJ398.
  • Analysis of cell growth using western blot, MTT assay, and cell-cycle analysis.

Main Results:

  • NVP-BGJ398 induced apoptosis through caspase-dependent (mitochondrial and non-mitochondrial) and caspase-independent pathways.
  • Cell-cycle arrest was observed in the G0/G1 phase.
  • Upregulation of programmed cell death 4 (PDCD4) and suppression of angiopoietin 2 (ANG2) were noted, indicating further anti-tumor mechanisms.

Conclusions:

  • NVP-BGJ398 effectively induces apoptosis in NSCLC cells via multiple pathways.
  • Small molecule FGFR inhibitors show promise for cancer treatment strategies.
Keywords:
ANG2NVP-BGJ398PDCD4Small molecule FGFR1 inhibitorcaspases

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