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Wild-type p53 gene expression induces granulocytic differentiation of HL-60
cells
S Soddu, G Blandino, G Citro, R Scardigli, G Piaggio, A Ferber, B Calabretta and A Sacchi
Molecular Oncogenesis Laboratory, Istituto Regina Elena CRS, Rome, Italy.
Overexpression of wild-type p53 gene in malignant cell lines has been shown
to inhibit cell proliferation in a number of cases. However, endogenous p53
protein seems to play little role in normal cell-cycle control as suggested
by the normal development of p53 null mice, and by the low p53 protein
levels expressed in most cell types. Recently, increased expression of
endogenous p53 protein has been observed during the cellular response to
DNA damage, as well as during differentiation of human hematopoietic cells.
To study the role of the p53 gene in hematopoietic differentiation, we
introduced the wild-type p53 gene or the temperature-sensitive p53(Val135)
mutant into p53-deficient HL-60 promyelocytic leukemia cells. Morphological
analysis, flow-cytometric determination of granulocytic or monocytic
surface markers, and ability to reduce nitroblue tetrazolium (NBT)
demonstrated that expression of exogenous wild-type p53 gene in HL-60 cells
induces differentiation through the granulocytic pathway. Proliferation and
cell-cycle analysis performed early after expression of wild-type p53
showed that induction of differentiation is not coupled with growth arrest,
which suggests that p53 is involved in differentiation independently of its
activity on the cell cycle.
Volume 83,
Issue 8,
pp. 2230-2237,
04/15/1994
Copyright © 1994 by The American Society of Hematology
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