Inhibition of insulin like growth factor II autocrine growth of Wilms' tumor by suramin in vitro and in vivo

Suramin was found to affect the Wilms' tumor (WT) cell line, W13, by inhibiting in vitro growth (half-maximal inhibitory dose (ID 50) = 11 μM), insulin like growth factor II (IGF-II) cell binding (ID 50 = 10μM) and IGF-II induced DNA synthesis (ID 50 = 8μM). In addition, suramin inhibited cross...

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Bibliographic Details
Published in:Cancer letters 1996-05, Vol.103 (1), p.49-56
Main Authors: Vincent, Timothy S., Hazen-Martin, Debra J., Garvin, A.Julian
Format: Article
Language:English
Subjects:
Animals
Antibodies - pharmacology
Antineoplastic agents
Antineoplastic Agents - pharmacology
Autocrine
Biological and medical sciences
Cell Division - drug effects
Cell Line
Chemotherapy
DNA, Neoplasm - biosynthesis
DNA, Neoplasm - drug effects
Dose-Response Relationship, Drug
Humans
Insulin like growth factor II
Insulin-Like Growth Factor II - antagonists & inhibitors
Insulin-Like Growth Factor II - metabolism
Insulin-Like Growth Factor II - pharmacology
Kidney Neoplasms - drug therapy
Kidney Neoplasms - pathology
Kinetics
Medical sciences
Mice
Mice, Nude
Mitotic Index
Pharmacology. Drug treatments
Radioligand Assay
Receptor, IGF Type 1 - antagonists & inhibitors
Receptor, IGF Type 1 - immunology
Receptor, IGF Type 1 - metabolism
Receptor, IGF Type 2 - antagonists & inhibitors
Receptor, IGF Type 2 - metabolism
Suramin
Suramin - pharmacology
Suramin - therapeutic use
Thymidine - metabolism
Transplantation, Heterologous
Tumor Cells, Cultured
Wilms Tumor - drug therapy
Wilms Tumor - pathology
Wilms' tumor
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Summary:Suramin was found to affect the Wilms' tumor (WT) cell line, W13, by inhibiting in vitro growth (half-maximal inhibitory dose (ID 50) = 11 μM), insulin like growth factor II (IGF-II) cell binding (ID 50 = 10μM) and IGF-II induced DNA synthesis (ID 50 = 8μM). In addition, suramin inhibited cross-linking of [ 125I]IGF-II to the type 1 IGF receptor (IGF1R) and type 2 IGF receptor (IGF2R). Disruption of IGF-II/IGF1R interaction appears to be the main mode of action of suramin since the suramin response was abolished in the presence of the IGF1R blocking antibody, αIR-3. When administered to athymic mice bearing W13 heterotransplants, suramin suppressed the linear tumor growth rate by 64%.
ISSN:0304-3835
1872-7980
DOI:10.1016/0304-3835(96)04186-9