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Carcinogenesis Advance Access published online on November 11, 2004
Carcinogenesis, doi:10.1093/carcin/bgh333
© 2004 by Oxford University Press
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Received August 20, 2004
Revised October 27, 2004
Accepted November 1, 2004

CANCER BIOLOGY

Down-regulation of the receptor for advanced glycation end-products (RAGE) supports non-small cell lung carcinoma

Babett Bartling 1*, Hans-Stefan Hofmann 1, Bernd Weigle 2, Rolf-Edgar Silber 1, and Andreas Simm 1

1 Clinic of Cardio-thoracic Surgery, Martin Luther University Halle-Wittenberg, Halle/Saale, Germany
2 Institute of Immunology, Technical University Dresden, Dresden, Germany

* To whom correspondence should be addressed.
Babett Bartling, E-mail: babett.bartling{at}medizin.uni-halle.de


  Abstract

The receptor for advanced glycation end-products (RAGE) is a transmembrane receptor of the immunoglobulin superfamily. Several ligands binding to RAGE have been identified, including amphoterin. Experimental studies have given rise to the discussion that RAGE and its interaction with amphoterin contribute to tumour growth and metastasis. However, none of the studies consider a differential transcription profile in cancer that might change the interpretation of the study results when comparing RAGE in tumours with histologically normal tissues. Here we show that RAGE is strongly reduced on mRNA and even more so on a protein level in non-small cell lung carcinomas compared with normal lung tissues. Down-regulation of RAGE correlates with higher tumour (TNM) stages but does not depend on the histological subtypes, squamous cell lung carcinoma and adenocarcinoma. Subsequent over-expression of full-length human RAGE in lung cancer cells (NCI-H358) showed a diminished tumour growth in some conditions. While the proliferation of RAGE-expressing cells was less than that of cells expressing the cytoplasmic domain deletion mutant {Delta}cytoRAGE or mock-transfected NCI-H358 in monolayer cultures, RAGE cells also formed smaller tumours in spheroid cultures and in vivo in athymic mice compared with {Delta}cytoRAGE cells. Moreover, we observed a more epithelial growth of RAGE- but also of {Delta}cytoRAGE-expressing cells on collagen layers, whereas mock NCI-H358 cells kept their tumour morphology. This observation was supported by immunofluorescence analyses demonstrating that RAGE preferentially localizes at the intercellular contact sites independent of the expression of the cytoplasmic domain. Thus, down-regulation of RAGE may be considered as a critical step in tissue reorganization and the formation of lung tumours.

Keywords: lung cancer; RAGE; proliferation; localization.
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