Publication: Suppression of growth of tumour cell lines in vitro and tumours in vivo by mistletoe lectins
Loading...
Date
2006
Authors
Pryme, I.F. ; Bardocz, S. ; Pusztai, A. ; Ewen, S.W.B.
item.page.secondaryauthor
item.page.director
Publisher
Murcia : F. Hernández
publication.page.editor
publication.page.department
DOI
item.page.type
info:eu-repo/semantics/article
Description
Abstract
A variety of studies have shown that
incubation of different tumour cell lines with mistletoe
lectins (MLs) in vitro has a marked cytotoxic effect. In
the concentration range of low cytotoxicity cell death
induced by ML-I is quantitatively due to apoptotic
processes. The first events observed being membrane
perforation and protusions. Simultaneous treatment of
certain tumour cells with MLs rendered them more
sensitive to induction of apoptosis by TNFa. The
immunomodulatory activity of ML-I was investigated by
measuring cytokine release and the results confirmed
that cytokine induction by the lectin is regulated at the
transcriptional level. ML-I has been shown to potentiate
the effect of chemotherapeutic drugs. In addition to an in
vitro effect a number of workers have demonstrated that
MLs suppress tumour growth in vivo. Mistletoe lectins
have been administered to animals locally to the tumour,
systemic, subcutaneously or by the oral route via the
diet. In many cases apoptosis was observed in the
tumour and instances where complete tumour ablation
has occurred have been reported. It has been
hypothesized that the anticancer efficacy of tumour
necrosis factor-alpha (TNFa) is potentiated by MLs
isolated from both European and Korean mistletoe.
There is accumulating evidence that both types of MLs are able to induce an anti-angiogenic response in the
host suggesting that the anti-metastatic effect observed
on a series of tumour cell lines in mice is in part due to
an inhibition of tumour-induced angiogenesis and in part
due to an induction of apoptosis.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Sin licencia Creative Commons.