Korean J Pediatr.  2010 Jul;53(7):753-758. 10.3345/kjp.2010.53.7.753.

Effect of p16 on glucocorticoid response in a B-cell lymphoblast cell line

• Kim SY
• Lee KY
• Jeong DC
• Kim HK

• KMID: 2073606
• DOI: http://doi.org/10.3345/kjp.2010.53.7.753

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.

Keyword

Glucocorticoid; Lymphoblast; p16

MeSH Terms

Apoptosis
B-Lymphocytes
Cell Cycle
Cell Line
Cell Survival
Cytoplasm
Dexamethasone
Lymphoma
Receptors, Glucocorticoid
RNA, Small Interfering
Transfection
Dexamethasone
RNA, Small Interfering
Receptors, Glucocorticoid