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Originally published as JHC exPRESS on April 16, 2007.
doi:10.1369/jhc.7A7176.2007
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Journal of Histochemistry and Cytochemistry
Volume 55 (8): 773-782, 2007
Copyright ©The Histochemical Society, Inc.

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

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

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)

Correspondence to: Dr. Jocelyne Fleury-Feith, Service d'Histologie et Biologie Tumorale, Hôpital Tenon, 4 rue de la chine, 75020, Paris, France. E-mail: jocelyne.fleury{at}tnn.aphp.fr

Lung resistance-related protein (LRP) is an integral part of the multidrug resistance (MDR) phenotype involved in cell resistance toward 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, whereas both proteins are associated with the MDR phenotype. (J Histochem Cytochem 55:773–782, 2007)

Key Words: lung resistance-related protein • bronchial cells • non-small cell lung cancer • DNA ploidy • flow cytometry • chromosome 16 • FISH


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