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Nargenicin enhances 1,25-dihydroxyvitamin D-3- and all-trans retinoic acid-induced leukemia cell differentiation via PKC beta I/MAPK pathways

Authors
Kim, Seung HyunYoo, Jin CheolKim, Tae Sung
Issue Date
1-Jun-2009
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Keywords
Nargenicin; Cell differentiation; 1,25-Dihydroxyvitamin D-3; All-trans retinoic acid; Protein kinase C; Mitogen-activated protein kinase
Citation
BIOCHEMICAL PHARMACOLOGY, v.77, no.11, pp.1694 - 1701
Indexed
SCIE
SCOPUS
Journal Title
BIOCHEMICAL PHARMACOLOGY
Volume
77
Number
11
Start Page
1694
End Page
1701
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/119840
DOI
10.1016/j.bcp.2009.03.004
ISSN
0006-2952
Abstract
A major goal in the treatment of acute myeloid leukemia (AML) is to achieve terminal differentiation and prevent drug resistance and side effects. Combined treatment with low doses of ATRA or 1,25-(OH)(2)D-3 that do not induce toxicity with another drug is one useful strategy for the treatment of AML. Actinomycetes are the well known sources of antibiotics and bioactive molecules. Previously, we isolated nargenicin from the culture broth of an actinomycete isolate, Nocardia sp. CS682. In this study, we evaluated the effects of nargenicin on cellular differentiation in a human myeloid leukemia HL-60 cell system. Nargenicin inhibited cell proliferation and induced HL-60 cell differentiation when administered in combination with 1,25-(OH)(2)D-3 or ATRA. In addition, western blot analyses and kinase inhibitor studies demonstrated that nargenicin primarily enhanced leukemia cell differentiation via PKC beta 1/MAPK pathways. The results of this study indicate that nargenicin has the ability to induce differentiation and suggest that it may be useful for the treatment of neoplastic diseases. (c) 2009 Elsevier Inc. All rights reserved.
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