Published ahead of print on October 28, 2004, doi:10.1165/rcmb.2004-0232OC
American Journal of Respiratory Cell and Molecular Biology. Vol. 32, pp. 65-71, 2005
© 2005 American Thoracic Society DOI: 10.1165/rcmb.2004-0232OC
The Consequences of Insulin-Like Growth Factors/Receptors Dysfunction in Lung Cancer
Jasminka Paveli ,
imun Kri anac,
Sanja Kapitanovi ,
Ljubomir Paveli ,
Miroslav Samar ija,
Fadila Pavi i ,
ime Spaventi,
Marko Jakopovi ,
Zlata Herceg-Ivanovi and
Kre imir Paveli
Division of Molecular Medicine, Rudjer Bo kovic 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 Bo kovic Institute, Bijeni ka 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
This article has been cited by other articles:

|
 |

|
 |
 
D. D. Karp, L. G. Paz-Ares, S. Novello, P. Haluska, L. Garland, F. Cardenal, L. J. Blakely, P. D. Eisenberg, C. J. Langer, G. Blumenschein Jr, et al.
Phase II Study of the Anti-Insulin-Like Growth Factor Type 1 Receptor Antibody CP-751,871 in Combination With Paclitaxel and Carboplatin in Previously Untreated, Locally Advanced, or Metastatic Non-Small-Cell Lung Cancer
J. Clin. Oncol.,
May 20, 2009;
27(15):
2516 - 2522.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. Dubey and C. A. Powell
Update in Lung Cancer 2008
Am. J. Respir. Crit. Care Med.,
May 15, 2009;
179(10):
860 - 868.
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
J. Shen, J. Liu, Y. Xie, B. A. Diwan, and M. P. Waalkes
Fetal Onset of Aberrant Gene Expression Relevant to Pulmonary Carcinogenesis in Lung Adenocarcinoma Development Induced by In Utero Arsenic Exposure
Toxicol. Sci.,
February 1, 2007;
95(2):
313 - 320.
[Abstract]
[Full Text]
[PDF]
|
 |
|
Copyright © 2005 American Thoracic Society.
|
|
|