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Science 2 November 1990:
Vol. 250. no. 4981, pp. 682 - 686
DOI: 10.1126/science.2237417
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Articles

Science, Vol 250, Issue 4981, 682-686
Copyright © 1990 by American Association for the Advancement of Science

articles

Down-regulation of LFA-1 adhesion receptors by C-myc oncogene in human B lymphoblastoid cells

G Inghirami, F Grignani, L Sternas, L Lombardi, DM Knowles, and R Dalla-Favera

Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.

The function of the c-myc gene and its role in tumorigenesis are poorly understood. In order to elucidate the role of c-myc oncogene activation in B cell malignancy, the phenotypic changes caused by the expression of c-myc oncogenes in human B lymphoblastoid cells immortalized by Epstein-Barr virus were analyzed. C-myc oncogenes caused the down-regulation of lymphocyte function-associated antigen-1 (LFA-1) adhesion molecules (alpha L/beta 2 integrin) and loss of homotypic B cell adhesion in vitro. Down-regulation of LFA-1 occurred by (i) posttranscriptional modulation of LFA-1 alpha L-chain RNA soon after acute c-myc induction, and (ii) transcriptional modulation in cells that chronically express c-myc oncogenes. Analogous reductions in LFA-1 expression were detectable in Burkitt lymphoma cells carrying activated c-myc oncogenes. Since LFA-1 is involved in B cell adhesion to cytotoxic T cells, natural killer cells, and vascular endothelium, these results imply functions for c-myc in normal B cell development and lymphomagenesis.


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