|Down-regulation of LFA-1 adhesion receptors by C-myc oncogene in human B lymphoblastoid cells.
|Year of Publication
|Inghirami G, Grignani F, Sternas L, Lombardi L, Knowles DM, Dalla-Favera R
|1990 Nov 02
|B-Lymphocytes, Cell Line, Cell Transformation, Neoplastic, Down-Regulation, Humans, Lymphocyte Function-Associated Antigen-1, Plasminogen Inactivators, Proto-Oncogene Proteins c-myc, Proto-Oncogenes
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.
|CA 37165 / CA / NCI NIH HHS / United States
CA 37295 / CA / NCI NIH HHS / United States
CA 48236 / CA / NCI NIH HHS / United States
Giorgio Inghirami, M.D.