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Reversible abrogation of IL‐3 dependence by an inducible H‐ras oncogene.
Author(s) -
Andrejauskas E.,
Moroni C.
Publication year - 1989
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1989.tb08396.x
Subject(s) - oncogene , transfection , biology , microbiology and biotechnology , cancer research , apoptosis , cell culture , genetics , cell cycle
Immortalized, interleukin‐3 (IL‐3)‐dependent mouse mast cells (PB‐3c) were transfected with a human activated c‐H‐ras gene under the transcriptional control of the mouse mammary tumor virus long terminal repeat. Addition of increasing amounts of dexamethasone resulted in a concentration‐dependent increase in expression of the H‐ras oncogene. The elevation of p21 ras protein concentrations was paralleled by progressive growth of the transfectants in the absence of exogenous IL‐3, leading to complete abrogation of growth‐factor requirement at high p21ras levels. The maintenance of the IL‐3‐independent state required the continuous expression of the H‐ras oncogene, since dexamethasone removal was followed by rapid cell death. Expression of the H‐ras oncogene induced PB‐3c cells to produce IL‐3 and granulocyte‐macrophage colony‐stimulating factor, suggesting that their IL‐3‐independent proliferation may be due to an autocrine mechanism.