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Expression of LY‐6.2 and Thy‐1 antigens on NIH 3T3 cells suppressed after transformation with activated human ras ‐oncogenes
Author(s) -
Ivanyi Dagmar,
Janssen Johannes W. G.,
Collard John G.
Publication year - 1986
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910380418
Subject(s) - transfection , antigen , microbiology and biotechnology , monoclonal antibody , biology , cell culture , 3t3 cells , antibody , cell , phenotype , malignant transformation , gene , cancer research , immunology , biochemistry , genetics
We have studied the expression of several cell surface antigens in NIH 3T3 cells after neoplastic transformation with activated human ras and myc oncogenes. The binding of monoclonal antibodies (MAbs), specific for mouse differentiation antigens Ly‐6.2, Thy‐1 and 9F3, to normal and transformed cells was assessed using a fluorescence‐activated cell sorter (FACS IV). Significant reduction of Ly‐6.2 and Thy‐1 antigen expression was detected in cells transformed with either the N‐ ras , Ki‐ ras or H‐ras oncogenes but not in c‐ myc transfected cells. 9F3 antigen expression remained at the original high level in all transfectants studied. Normal levels of Ly‐6.2 and Thy‐1 expression reappeared in revertants derived from: unstable ras ‐transfectants. These data indicate that ras sequences did not preferentially transform cells that were deficient in Ly‐6.2 and Thy‐l antigens. It was also shown that the reduced binding of anti‐Ly‐6.2 antibodies to ras ‐transfectants was not due to a masking effect of increased cell‐surface sialylation occurring in ras ‐transfected cell lines. Other possible explanations of the detected phenotypic changes are discussed. The results extend the range of tumor‐associated membrane alterations in NIH 3T3 cells following transfection with human tumor DNA containing activated ras oncogenes by a hitherto unreported alteration in the expression of Ly‐6 and Thy‐1 antigens.