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Angiogenesis induced by urothelial cells (HCV-29) and their v-ras and v-raf transfectants

M Przybyszewska1, J Miłoszewska, P Janik

  • 1Department of Cell Biology, The Maria Sklodowska-Curie Cancer Center, Warsaw, Poland.

Cancer Letters
|December 16, 1998
PubMed

Insights

V-raf gene transfection significantly enhanced angiogenesis in human urothelial cells. This increased blood vessel formation correlated with higher vascular endothelial growth factor (VEGF) levels, indicating a key role for VEGF in this process.

Area of Science:

  • Oncology
  • Cell Biology
  • Biotechnology

Background:

  • Angiogenesis is crucial for tumor growth and metastasis.
  • Human urothelial cells (HCV-29) are relevant models for bladder cancer research.
  • Genetic modification can alter cellular angiogenic potential.

Purpose of the Study:

  • To investigate the angiogenic capacity of human urothelial cells (HCV-29) and their genetically modified variants.
  • To determine the impact of v-ras and v-raf oncogene transfection on cellular angiogenesis.
  • To explore the correlation between angiogenic activity and vascular endothelial growth factor (VEGF) expression.

Main Methods:

  • In vivo angiogenesis assays were performed.
  • Reverse transcription polymerase chain reaction (RT-PCR) was used to measure VEGF mRNA.
  • Western blotting was employed to quantify VEGF protein levels.

Main Results:

  • V-raf-transfected cells exhibited the most pronounced in vivo angiogenesis.
  • Parental HCV-29 cells showed the lowest degree of neovascularization.
  • Increased angiogenesis correlated positively with both VEGF mRNA and protein expression.

Conclusions:

  • Transfection with v-raf oncogene significantly enhances the angiogenic potential of human urothelial cells.
  • VEGF is a key mediator of the observed increase in angiogenesis.
  • These findings contribute to understanding the role of oncogenes in tumor angiogenesis.

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