Nerve growth factor from cobra venom inhibits the growth of Ehrlich tumor in mice

Toxins (Basel). 2014 Feb 26;6(3):784-95. doi: 10.3390/toxins6030784.

Abstract

The effects of nerve growth factor (NGF) from cobra venom (cvNGF) on growth of Ehrlich ascites carcinoma (EAC) cells inoculated subcutaneously in mice have been studied. The carcinoma growth slows down, but does not stop, during a course of cvNGF injections and restores after the course has been discontinued. The maximal anti-tumor effect has been observed at a dose of 8 nmoles cvNGF/kg body weight. cvNGF does not impact on lifespan of mice with grafted EAC cells. K252a, a tyrosine kinase inhibitor, attenuates the anti-tumor effect of cvNGF indicating the involvement of TrkA receptors in the process. cvNGF has induced also increase in body weight of the experimental animals. In overall, cvNGF shows the anti-tumor and weight-increasing effects which are opposite to those described for mammalian NGF (mNGF). However in experiments on breast cancer cell line MCF-7 cvNGF showed the same proliferative effects as mNGF and had no cytotoxic action on tumor cells in vitro. These data suggest that cvNGF slows down EAC growth via an indirect mechanism in which TrkA receptors are involved.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use*
  • Carbazoles / pharmacology
  • Carcinoma, Ehrlich Tumor / drug therapy*
  • Carcinoma, Ehrlich Tumor / metabolism
  • Carcinoma, Ehrlich Tumor / pathology
  • Cell Proliferation / drug effects
  • Elapid Venoms*
  • Female
  • Humans
  • Indole Alkaloids / pharmacology
  • MCF-7 Cells
  • Mice
  • Nerve Growth Factor / pharmacology
  • Nerve Growth Factor / therapeutic use*
  • Protein Kinase Inhibitors / pharmacology
  • Receptor, trkA / antagonists & inhibitors
  • Receptor, trkA / metabolism
  • Tumor Burden / drug effects

Substances

  • Antineoplastic Agents
  • Carbazoles
  • Elapid Venoms
  • Indole Alkaloids
  • Protein Kinase Inhibitors
  • Nerve Growth Factor
  • staurosporine aglycone
  • Receptor, trkA