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[Effect of nitric oxide derived from endothelial nitric oxide synthase on tumor angiogenesis]

Kai Mei1, Xiao-Hong Cai, Lei Du

  • 1Department of Medical Oncology,Sichuan Cancer Hospital, Chengdu, Sichuan 610041, People's Republic of China. meikai1973@yahoo.com.cn

Chinese Journal of Cancer
|December 30, 2009
PubMed
Abstract

Insights

Nitric oxide (NO) derived from endothelial nitric oxide synthase (eNOS) inhibits tumor growth and angiogenesis. This effect may involve suppressing endothelial progenitor cells (EPCs) mobilization or homing via VEGF signaling.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) is implicated in tumor angiogenesis, but findings are conflicting.
  • Understanding NO's role in tumor vascularization is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the precise effect of NO on tumor angiogenesis and elucidate its underlying mechanisms.
  • To clarify the controversial role of NO in tumor development.

Main Methods:

  • Lewis lung cancer cells were used to establish tumors in C57BL/6 mice.
  • Mice were divided into three groups: eNOS gene-transfected (NO group), L-NAME treated (eNOS antagonist), and control.
  • Measurements included plasma NO, peripheral blood endothelial progenitor cells (EPCs), tumor vessel density, CD133+ cells, and VEGF-VEGFR expression.

Main Results:

  • Tumor volume was significantly reduced in both the eNOS and L-NAME groups compared to controls.
  • eNOS gene transfection increased NO production but decreased tumor vessel density and CD133+ cells.
  • L-NAME treatment decreased NO levels, reduced tumor vessel density, and lowered EPCs and CD133+ cells in peripheral blood and tumors.

Conclusions:

  • NO derived from eNOS inhibits tumor angiogenesis and growth.
  • This inhibition may occur by suppressing endothelial progenitor cell (EPC) mobilization or homing through VEGF-VEGFR interactions.

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