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[Cancer Research 53, 1475-1479, April 1, 1993]
© 1993 American Association for Cancer Research
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Overexpression of a Mr 110,000 Vesicular Protein in Non-P-Glycoprotein-mediated Multidrug Resistance1

Rik J. Scheper2, Henricus J. Broxterman3, George L. Scheffer, Patricia Kaaijk, William S. Dalton, Theodorus H. M. van Heijningen, Coen K. van Kalken, Marilyn L. Slovak, Elisabeth G. E. de Vries, Paul van der Valk, Chris J. L. M. Meijer and Herbert M. Pinedo

Departments of Pathology [R. J. S., G. L. S., P. K., P. v. d. V., C. J. L. M. M.] and Oncology [H. J. B., T. H. M. v. H., C. K. v. K., H. M. P.], Free University Hospital, De Boelelaan 1117, 1081 HV Amsterdam, the Netherlands; Arizona Cancer Center, Tucson, Arizona 85724 [W. S. D.]; Department of Cytogenetics, City of Hope, National Medical Center, Duarte, California 91010 [M. L. S.]; and Division of Medical Oncology, University Hospital, Groningen, 9713 EZ, the Netherlands [E. G. E. d. V.]

A Mr110,000 protein (p110) is overexpressed in P-glycoprotein-negative multidrug-resistant tumor cell lines of different histogenetic origins. These cell lines show an ATP-dependent drug accumulation defect, suggesting the presence of drug transporter molecules different from P-glycoprotein. Immunohistochemical staining with a p110-specific monoclonal antibody (LRP-56) showed that, like P-glycoprotein, the molecule has a high expression in normal epithelial cells and tissues chronically exposed to xenobiotics and potentially toxic agents, such as bronchial cells, cells lining the intestines, and kidney tubules. Staining of LRP-56 is primarily cytoplasmic, in a coarsely granular fashion, indicating that it reacts with a molecule closely associated with vesicular/lysosomal structures. Involvement of p110 in the energy-dependent drug transport process present in the cell lines is unknown.

1 This work was supported in part by the Bristol-Myers Squibb Research grant program.

2 To whom requests for reprints should be addressed.

3 Fellow of the Royal Netherlands Academy of Arts and Sciences.

Received 12/23/92. Accepted 2/18/93.




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