PMID: 9537584Apr 16, 1998Paper

Expression of a kinase-deficient IGF-I-R suppresses tumorigenicity of rhabdomyosarcoma cells constitutively expressing a wild type IGF-I-R

International Journal of Cancer. Journal International Du Cancer
T KalebicLee J Helman

Abstract

Previous results have shown that the insulin-like growth factor type I receptor (IGF-I-R) plays a critical role in the control of rhabdomyosarcoma (RMS) growth. The purpose of this study was to investigate whether a mutated IGF-I-R, when expressed in RMS cells, may interfere with the function of the endogenous wild-type IGF-I-R. We also examined whether the expression of a mutated IGF-I-R may induce phenotypic changes in RMS cells. We used here the mutated IGF-I-R with a lysine to arginine residue 1003 substitution, called IGF-I-KR, which carries a mutation in the ATP-binding domain of the intracellular beta subunit, while the extracellular, ligand binding alpha subunit remains unchanged. We observed that the expression of this mutated IGF-I-KR markedly decreased the response of RMS cells to stimulation with IGF-I. While stimulation with IGF-I increases the autophosphorylation of IGF-I-R in the parent cells, stimulation with IGF-I failed to produce a comparable increase in autophosphorylation in the cells expressing the mutated IGF-I-KR. We also observed a decreased plating efficiency of cells expressing the mutated IGF-I-KR. Consistently, a decrease of RMS growth in vivo was observed in an animal model. Our data suggest that t...Continue Reading

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Citations

Oct 12, 2012·Journal of Mammary Gland Biology and Neoplasia·Yuzhe Yang, Douglas Yee
Oct 27, 2005·Cancer Biotherapy & Radiopharmaceuticals·Shakeel ModakNai-Kong V Cheung
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Feb 4, 2012·Current Oncology Reports·Patrick A Thompson, Murali Chintagumpala
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Dec 4, 2010·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·R BagatellL Gore

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