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[Cancer Research 60, 1961-1967, April 1, 2000]
© 2000 American Association for Cancer Research

Molecular Biology and Genetics

LRP-DIT, a Putative Endocytic Receptor Gene, Is Frequently Inactivated in Non-Small Cell Lung Cancer Cell Lines1

Chun-Xiang Liu, Simone Musco, Natalia M. Lisitsina, Eva Forgacs, John D. Minna and Nikolai A. Lisitsyn2

Laboratory of Cancer Genetics, Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 [C-X. L., S. M., N. M. L., N. A. L.], and Hamon Center for Therapeutic Oncology Research, The University of Texas Southwestern Medical Center, Dallas, Texas 75235 [E. F., J. D. M.]

A variety of studies suggest that allelic losses at chromosome 2q are associated with aggressive behavior of various forms of human neoplasia. Using a probe to detect homozygous deletions on chromosome 2q21.2 in kidney and bladder cancer cell lines, we identified a new candidate tumor suppressor gene, lipoprotein receptor-related protein-deleted in tumors (LRP-DIT). The predicted LRP-DIT product of 4599 amino acids has extensive homology to a gigantic receptor, LRP1, which mediates endocytosis of multiple proteins from the cell surface. Homozygous deletions in LRP-DIT were detected in 17% (4 of 23) of non-small cell lung cancer (NSCLC) cell lines. The expression of only abnormal transcripts missing portions of the LRP-DIT sequence was demonstrated in an additional 30% (11 of 36) of NSCLC lines. Finally, a missense mutation at codon 3157 was detected in one of four NSCLC lines tested for the large open reading frame. In contrast, no LRP-DIT alterations were identified in a major fraction of SCLC cell lines, indicating that this gene is preferentially inactivated in one histological type of lung cancer. Our data suggest that inactivation of LRP-DIT occurs in at least 40% of NSCLC lines and thus may play an important role in tumorigenesis of NSCLCs.




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