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Published ahead of print on October 28, 2004, doi:10.1165/rcmb.2004-0232OC

Am. J. Respir. Cell Mol. Biol., Volume 32, Number 1, January 2005, 65-71

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Submitted on July 22, 2004
Revised on October 22, 2004

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

Jasminka Pavelic1*, Simun Krizanac1, Sanja Kapitanovic1, Ljubomir Pavelic2, Miroslav Samarzija2, Fadila Pavicic2, Sime Spaventi3, Marko Jakopovic2, Zlata Herceg-Ivanovi2, and Kresimir Pavelic1

1 Division of Molecular Medicine, Rudjer Boskovic Institute, Zagreb, Croatia (Hrvatska), 2 Clinical Hospital of Pulmonary Diseases Jordanovac, Zagreb, Croatia (Hrvatska), 3 Division of Medical Sciences, Croatian Academy of Sciences and Arts, Zagreb, Croatia (Hrvatska)

* To whom correspondence should be addressed. E-mail: jpavelic{at}irb.hr.

The aim of this study was to investigate the consequences of IGFs/IGF receptors dysfunction in lung carcinomas. A correlation between increased expression (at mRNA and protein levels) for both, IGF 1 and IGF 1R, and decreased apoptosis was 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 and a mutation in another allele. All four squamous cell carcinoma samples also expressed LOH/mutation in the M6P/IGF 2R gene. The {alpha}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 {alpha}IR3 that inhibits the activity of IGF 1 receptors. Our findings suggest that disruption of the IGFs/IGF receptors axis is involved in lung cancer formation.




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