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The BCR-ABL oncogene requires both kinase activity and src-homology 2
domain to induce cytokine secretion
SM Anderson and J Mladenovic
Department of Pathology, Colorado Health Science Center, Denver 80262, USA.
Expression of either the BCR-ABL or the v-abl oncogene in the factor-
dependent murine myeloid cell line FDCP-1 results in growth factor
independence. Studies with temperature-sensitive mutants of v-abl show that
this growth factor independence is oncogene dependent. Likewise, cells
expressing a kinase inactive mutant of BCR-ABL did not grow in the absence
of interleukin-3 (IL-3). Conditioned media from cells expressing either
v-abl or BCR-ABL contained growth factor(s) capable of stimulating the
proliferation of uninfected FDCP-1 cells. Based on enzyme-linked
immunosorbent assay studies and antibody neutralization studies, the major
growth factor present in these conditioned media is IL-3. Because of the
importance of SH2 domains in regulating substrate interactions, we examined
the ability of SH2 deletion mutants in BCR- ABL to induce growth factor
independence. Cells expressing a mutant of BCR-ABL lacking the SH2 domain
were growth factor independent; however, they did not secrete growth
factors. This finding suggests that while IL-3 produced by cells infected
with BCR-ABL may contribute to autocrine or paracrine growth factor
independence, expression of an activated tyrosine kinase alone may be able
to induce growth factor independence. Furthermore, the secretion of
cytokines maybe correlated with a specific region of the BCR-ABL oncogene,
suggesting that activation (phosphorylation) of specific substrates may be
critical for transcriptional activation of cytokine genes.
Volume 87,
Issue 1,
pp. 238-244,
01/01/1996
Copyright © 1996 by The American Society of Hematology
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