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19 February 1998, Volume 16, Number 7, Pages 915-923
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Article
Down-regulation of nucleophosmin/B23 during retinoic acid-induced differentiation of human promyelocytic leukemia HL-60 cells
Chen Ya Hsu1,2,b and Benjamin YM Yung2,a

1Graduate Institute of Pharmacology, National Yang Ming University, Taiwan, Republic of China

2Cancer Biochemistry Laboratory, Department of Pharmacology, Chang Gung Medical & Engineering College, 259 Wen-Hwa 1st Road, Kwei-San, Tao-Yuan 333, Taiwan, Republic of China

aAuthor for correspondence

bCY Hsu is a graduate student at the Graduate Institute of Pharmacology, National Yang Ming University. This work is in partial fulfilment of the requirements for her Master of Science degree

Abstract

Human promyelocytic leukemia HL-60 cells were induced to undergo granulocytic differentiation by treatment with retinoic acid (RA, 10 muM, 1-5 days). The steady-state level of nucleophosmin/B23 mRNA decreased during the RA-induced differentiation. There was also decrease in the level of total cellular nucleophosmin/B23 protein during the RA-induced differentiation. Stabilization and nuclear run-on assays indicate that the decrease in nucleophosmin/B23 mRNA in RA-treated HL-60 cells was transcriptionally regulated. Unlike c-myc mRNA, there was virtually no decline of nucleophosmin/B23 mRNA during the growth arrest by serum-starvation. The decrease in nucleophosmin/B23 mRNA expression in HL-60 cells subsequent to retinoic acid treatment can thus be attributed to cellular differentiation rather than the growth arrest induced by RA. Nucleophosmin/B23 antisense oligomer treatment significantly potentiated RA-induced cellular differentiation. Results of this study suggest that nucleophosmin/B23 is one of the key elements in the down-regulation of nucleolar function for cellular differentiation.

Keywords

Nucleophosmin/B23; retinoic acid; HL-60 differentiation

Received 11 July 1997; revised 30 September 1997; accepted 30 September 1997
19 February 1998, Volume 16, Number 7, Pages 915-923
Table of contents    Previous  Abstract  Next   Article  PDF