期刊
LEUKEMIA RESEARCH
卷 35, 期 12, 页码 1644-1648出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.leukres.2011.07.002
关键词
Glucocorticoid resistance; 11 beta-Hydroxysteroid dehydrogenase 2; Acute lymphoblastic leukemia
资金
- Uehara Memorial Foundation
Synthetic glucocorticoids (GCs) form a crucial first-line treatment for childhood acute lymphoblastic leukemia (ALL). However prolonged GC therapy frequently leads to GC-resistance with an unclear molecular mechanism. 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) 2 inactivates GCs within cells. Here, we show the association between GC sensitivity and 11 beta-HSD2 expression in human T-cell leukemic cell lines. 11 beta-HSD2 mRNA and protein levels were considerably higher in GC-resistant MOLT4F cells than in GC-sensitive CCRF-CEM cells. The 11 beta-HSD inhibitor, carbenoxolone pre-treatment resulted in greater cell death with prednisolone assessed by methyl-thiazol-tetrazolium assay and caspase-3/7 assay, suggesting that 11 beta-HSD2 is a cause of GC-resistance in ALL. (C) 2011 Elsevier Ltd. All rights reserved.
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