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Loss of EGF binding and cation transport response during differentiation of mouse neuroblastoma cells
Author(s) -
Mummery C. L.,
van der Saag P. T.,
de Laat S. W.
Publication year - 1983
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240210108
Subject(s) - epidermal growth factor , stimulation , receptor , neuroblastoma , clone (java method) , microbiology and biotechnology , dna synthesis , cell culture , biology , endocrinology , chemistry , biophysics , medicine , in vitro , biochemistry , dna , genetics
Mouse neuroblastoma cells (clone N1E‐115) differentiate in culture upon withdrawal of serum growth factors and acquire the characteristics of neurons. We have shown that exponentially growing N1E‐115 cells possess functional epidermal growth factor (EGF) receptors but that the capacity for binding EGF and for stimulation of DNA synthesis is lost as the cells differentiate. Furthermore, in exponentially growing cells, EGF induces a rapid increase in amiloride‐sensitive Na + influx, followed by stimulation of the (Na + ‐K + )ATPase, indicating that activation of the Na + /H + exchange mechanism in N1E‐115 cells [1] may be induced by EGF. The ionic response is also lost during differentiation, but we have shown that the stimulation of both Na + and K + influx is directly proportional to the number of occupied receptors in all cells whether exponentially growing or differentiating, thus only indirectly dependent on the external EGF concentration. The linearity of the relationships indicates that there is no rate‐limiting step between EGF binding and the ionic response. Our data would suggest that as neuroblastoma cells differentiate and acquire neuronal properties, their ability to respond to mitogens, both biologically and in the activation of cation transport processes, progressively decreases owing to the loss of the appropriate receptors.