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Signal Transduction through the EGF Receptor Transfected in IL-3--Dependent Hematopoietic Cells
Jacalyn H. Pierce, Marco Ruggiero, Timothy P. Fleming, Pier Paolo Di Fiore, Joel S. Greenberger, Lyuba Varticovski, Joseph Schlessinger, Giovanni Rovera and Stuart A. Aaronson
New Series, Vol. 239, No. 4840 (Feb. 5, 1988), pp. 628-631
Published by: American Association for the Advancement of Science
Stable URL: http://www.jstor.org/stable/1700185
Page Count: 4
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An expression vector for the epidermal growth factor (EGF) receptor was introduced into the 32D myeloid cell line, which is devoid of EGF receptors and absolutely dependent on interleukin-3 (IL-3) for its proliferation and survival. Expression of the EGF receptor conferred the ability to utilize EGF for transduction of a mitogenic signal. When the transfected cells were propagated in EGF, they exhibited a more mature myeloid phenotype than was observed under conditions of IL-3--directed growth. Moreover, exposure to EGF led to a rapid stimulation of phosphoinositide metabolism, while IL-3 had no detectable effect on phosphoinositide turnover either in control or EGF receptor-transfected 32D cells. Although the transfected cells exhibited high levels of functional EGF receptors, they remained nontumorigenic. In contrast, transfection of v-erbB, an amino-terminal truncated form of the EGF receptor with constitutive tyrosine kinase activity, not only abrogated the IL-3 growth factor requirement of 32D cells, but caused them to become tumorigenic in nude mice. These results show that a naive hematopoietic cell expresses all of the intracellular components of the EGF-signaling pathway necessary to evoke a mitogenic response and sustain continuous proliferation.
Science © 1988 American Association for the Advancement of Science