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.
Highlights
Nerve growth factor (NGF) is a neurotrophin participating in processes of growth, differentiation, and survival of neurons both in the peripheral and the central nervous systems [1]
In this paper we present the detailed studies of cobra venom NGF (cvNGF) effects on growth of Ehrlich ascites carcinoma (EAC) cells in vivo and show the involvement of TrkA receptors in the suppression process
The existing data about NGF influence on the breast cancer are controversial: on the one hand, it has been shown that mammalian NGF (mNGF) stimulates the proliferation of breast cancer cell lines [9], while on the other the elevated level of NGF receptor tropomyosin-related kinase (Trk)-A correlates with survival of patient with breast cancer [10]
Summary
Nerve growth factor (NGF) is a neurotrophin participating in processes of growth, differentiation, and survival of neurons both in the peripheral and the central nervous systems [1]. Recombinant mNGF is on the market, it is extremely expensive Neurotrophins exert their action through the specific receptors - tropomyosin-related kinase (Trk) subfamily of receptor tyrosine kinases. In mammals, these receptors are presented by the three members and exhibit ligand selectivity: NGF is the preferential high-affinity ligand for TrkA. These receptors are presented by the three members and exhibit ligand selectivity: NGF is the preferential high-affinity ligand for TrkA It is a ligand for p75 neurotrophin receptor (p75NTR), a member of the tumor necrosis factor receptor superfamily, that binds all neurotrophins with similar affinities, regulates apoptosis and has no tyrosine kinase activity (see review [6]). In this paper we present the detailed studies of cvNGF effects on growth of EAC cells in vivo and show the involvement of TrkA receptors in the suppression process
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