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ORIGINAL ARTICLE
Korean J Pediatr 2010 July;53(7) :753-758.
doi:https://doi.org/10.3345/kjp.2010.53.7.753
Effect of p16 on glucocorticoid response in a B-cell lymphoblast cell line
Sun-Young Kim (Kim SY)1, Kyung-Yil Lee (Lee KY)2, Dae-Chul Jeong (Jeong DC)2, Hak-Ki Kim (Kim HK)2
1Department of Pediatrics, College of Medicine, Hanyang University, Seoul, Korea
2Department of Pediatrics, College of Medicine, The Catholic University of Korea, Seoul, Korea
Corresponding Author: Kyung-Yil Lee ,Email: leekyungyil@catholic.ac.kr
Copyright © 2010 by The Korean Pediatric Society
ABSTRACT
Purpose : It has been suggested that p16 has a role in glucocorticoid (GC)-related apoptosis in leukemic cells, but the exact mechanisms have yet to be clarified. We evaluated the relationship between the GC response and p16 expression in a lymphoma cell line. Methods : We used p16 siRNA transfection to construct p16-inactivated cells by using the B-cell lymphoblast cell line NC-37. We compared glucocorticoid receptor (GR) expression, apoptosis, and cell viability between control (p16+ NC-37) and p16 siRNA-transfected (p16– NC- 37) cells after a single dose of dexamethasone (DX). Results : In both groups, there was a significant increase in cytoplasmic GR expression, which tended to be higher for p16+ NC-37 cells than for p16– NC37 cells at all times, and the difference at 18 h was significant (P<0.05). Similar patterns of early apoptosis were observed in both groups, and late apoptosis occurred at higher levels at 18 h when the GR had already been downregulated (P<0.05). Cell viability decreased in both groups but the degree of reduction was more severe in p16+ NC-37 cells after 18 h (P<0.05). Conclusion : These results suggest a relationship between GR expression and cell cycle inhibition, in which the absence of p16 leads to reduced cell sensitivity to DX.
Keywords: Glucocorticoid | Lymphoblast | p16
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