Related Experiment Video
Updated: Jul 20, 2026
The Corneal Micropocket Assay: A Model of Angiogenesis in the Mouse Eye
Published on: August 16, 2014
Enhanced expression of VEGF following bFGF inhibition in non-small cell lung cancer cell lines
Hartmut Kuhn1, Jana Konrad, Silke Holtz
1Department of Respiratory Medicine, University of Leipzig, Germany. kuhnh@medizin.uni-leipzig.de
Abstract:
Inhibition of basic fibroblast growth factor (bFGF) leads to decreased proliferation of non-small cell lung cancer (NSCLC) cell lines. Although it is well known that bFGF stimulates vascular endothelial growth factor (VEGF) secretion, the influence of bFGF-inhibition is unclear. We therefore investigated the influence of bFGF inhibition on VEGF gene expression and secretion in NSCLC cell lines. In our experiments we demonstrated that inhibition of bFGF gene and protein expression induced increased secretion of VEGF. We also observed an increase of VEGF gene expression in these cells. Furthermore, inhibition of bFGF activated the p42/p44 mitogen-activated protein kinase (MAPK). These results demonstrate that inhibition of bFGF appears to stimulate VEGF production in a p42/44 MAPK-dependent manner. These findings suggest that inhibition of bFGF alone is not a promising strategy to inhibit angiogenesis.
Insights
Inhibiting basic fibroblast growth factor (bFGF) in non-small cell lung cancer (NSCLC) paradoxically increased vascular endothelial growth factor (VEGF) production. This suggests bFGF inhibition alone is not effective for blocking tumor angiogenesis.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Basic fibroblast growth factor (bFGF) is known to decrease non-small cell lung cancer (NSCLC) proliferation.
- The effect of bFGF inhibition on vascular endothelial growth factor (VEGF) secretion in NSCLC is not well understood.
Purpose of the Study:
- To investigate the impact of bFGF inhibition on VEGF gene expression and secretion in NSCLC cell lines.
- To elucidate the signaling pathways involved in the bFGF-VEGF relationship in NSCLC.
Main Methods:
- Inhibition of bFGF gene and protein expression in NSCLC cell lines.
- Measurement of VEGF gene expression and secretion.
- Analysis of mitogen-activated protein kinase (MAPK) pathway activation, specifically p42/p44 MAPK.
Main Results:
- Inhibition of bFGF led to increased VEGF secretion in NSCLC cells.
- VEGF gene expression was also found to increase following bFGF inhibition.
- Activation of the p42/p44 MAPK pathway was observed upon bFGF inhibition.
Conclusions:
- bFGF inhibition stimulates VEGF production in NSCLC cells in a p42/44 MAPK-dependent manner.
- Targeting bFGF alone is unlikely to be an effective strategy for inhibiting angiogenesis in NSCLC.
- Further research is needed to understand the complex interplay between bFGF and VEGF in lung cancer progression.
