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Antisense inhibition of c-fes proto-oncogene blocks PMA-induced macrophage
differentiation in HL60 and in FDC-P1/MAC-11 cells
R Manfredini, R Balestri, E Tagliafico, F Trevisan, M Pizzanelli, A Grande, D Barbieri, P Zucchini, G Citro, C Franceschi and S Ferrari
Department of Biomedical Sciences, University of Modena, Italy.
To gain some insight into the role of c-fes in macrophage differentiation,
we have analyzed the ability of HL60 leukemic promyelocytic cells and
FDC-P1/MAC-11 murine myeloid precursor cells to differentiate in response
to phorbol esters after inhibition of c-fes function. Fes inactivation has
been obtained by using oligodeoxynucleotides (ODN) complementary to the 5'
region of c-fes mRNA and to 5' splice junctions of c-fes primary
transcript. After 5 days (d) in culture, in several separate experiments
performed with different ODN preparations, a complete inhibition of c-fes
expression was observed in HL60 and in FDC-P1/MAC-11 cells. No perturbation
of cell growth was evident in our experimental conditions in both cell
lines after c-fes inhibition. Furthermore, in HL60 cells lacking c-fes
product, an almost complete downregulation of the alpha 4 beta 1
fibronectin receptor occurred. However, in both cell lines, the induction
of macrophage differentiation by phorbol esters resulted in an almost
complete maturation arrest as evaluated by morphological, cytochemical,
immunological criteria, and by the cytofluorimetric cell cycle analysis. A
loss of the adhesion capacity of both myeloid cell lines, when compared to
terminally differentiated macrophages, was also observed. These results
suggest that HL60 and FDC-P1/MAC-11 cells, when treated with phorbol
12-myristate 13-acetate, require c-fes protein expression to activate the
genetic program underlying macrophage differentiation.
Volume 89,
Issue 1,
pp. 135-145,
01/01/1997
Copyright © 1997 by The American Society of Hematology
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