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JHC exPRESS: First Published April 16, 2007. doi:10.1369/jhc.7A7176.2007
Journal of Histochemistry and Cytochemistry
Copyright © 2007 Bouhamyia et al.

A more recent version of this article appeared on August 1, 2007.
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Articles

Immunolocalization and Cell Expression of Lung Resistance-related Protein (LRP) in Normal and Tumoral Human Respiratory Cells

Lamiaâ Bouhamyia 1, Sandra Chantot-Bastaraud 1, Sakina Zaidi 1, Patricia Roynard 1, Claudie Prengel 1, Jean-François Bernaudin 1 and Jocelyne Fleury-Feith 1*

1 Service d’Histologie et Biologie Tumorale (LB,SZ,PR,CP,J-FB,JF-F) and Service d’Histologie-Cytogénétique (SC-B), Hôpital Tenon (AP-HP), Paris, France, and UPRES EA3499, Université Pierre et Marie Curie, Paris, France (LB,SZ,PR,CP,J-FB,JF-F)

* To whom correspondence should be addressed. E-mail: jocelyne.fleury{at}tnn.aphp.fr.

Submitted on January 1, 2007
Accepted on 22 March 2007


  Abstract
LRP is an integral part of the multidrug resistance (MDR) phenotype involved in cell resistance towards xenobiotics or chemotherapy. The aim of this study was to compare the intracellular localization and cell expression of LRP in normal bronchial cells and their tumoral counterparts from non small cell lung cancer (NSCLC). LRP expression was also investigated concurrently with DNA ploidy and chromosome 16 (lrp gene locus) aberrations. Confocal microscopy showed that LRP localization was exclusively intracytoplasmic regardless of the cell type and was never observed in the nuclear pore complex. Flow cytometry demonstrated a similar level of LRP expression in normal bronchial cells and in cancer cells from NSCLC samples. FISH analysis performed to evaluate the number of chromosome 16 and lrp loci, demonstrated a significant gain of chromosome 16 in DNA-aneuploid tumors. Furthermore, we did not find any link between LRP expression and DNA ploidy status or chromosome 16 number. These results suggest that LRP expression observed in NSCLC, maintained through the carcinogenesis process of respiratory cells, is not altered by the increased number of copies of chromosome 16 and probably controlled by mechanisms different from those of MRP1 expression, while both proteins are associated with the MDR phenotype.

Key Words: lung resistance-related protein, bronchial cells, non-small-cell lung cancer, DNA ploidy, flow cytometry, chromosome 16, fluorescent in situ hybridization


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