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The Consequences of Insulin-Like Growth Factors/Receptors Dysfunction in Lung Cancer

Jasminka Paveli, imun Krianac, Sanja Kapitanovi, Ljubomir Paveli, Miroslav Samarija, Fadila Pavii, ime Spaventi, Marko Jakopovi, Zlata Herceg-Ivanovi and Kreimir Paveli

Division of Molecular Medicine, Rudjer Bokovic Institute; Clinical Hospital of Pulmonary Diseases Jordanovac; and Croatian Academy of Sciences and Arts, Division of Medical Sciences, Zagreb, Croatia

Correspondence and requests for reprints should be addressed to Professor Jasminka Paveli, Division of Molecular Medicine, Rudjer Bokovic Institute, Bijenika 54, P. Box 180, HR-10002 Zagreb, Croatia. E-mail: jpavelic{at}irb.hr

The aim of this study was to investigate the consequences of insulin-like growth factors (IGF) and IGF receptor dysfunction in lung carcinomas. A correlation between increased expression (at mRNA and protein levels) for IGF-1 and IGF-1R and decreased apoptosis were found in large-cell carcinomas and adenocarcinomas. In 40% of informative adenocarcinomas expressing the highest values of IGF-2 and Ki-67 proteins, M6P/IGF-2R gene had LOH at one allele and a mutation in another allele. All four squamous cell carcinoma samples expressed LOH/mutation in the M6P/IGF-2R gene. The IR3 strongly diminished proliferation and increased apoptosis in cultures established from squamous cell carcinomas overexpressing IGF-2 and IGF-1R. Telomerase activity was assessed in four squamous cell carcinomas. Cell treatment with IGF-1 increased telomerase activity. The opposite was observed when the cells were treated with IR3, which inhibits the activity of IGF-1 receptors. Our findings suggest that disruption of the IGF/IGF receptors axis is involved in lung cancer formation.

Key Words: insulin-like growth factors • receptors • lung cancer

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