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Title 

(-)-Syringaresinol inhibits proliferation of human promyelocytic HL-60 leukemia cells via G1 arrest and apoptosis

Authors 

Bo Young ParkSei Ryang OhKyung Seop AhnOk Kyong KwonHyeong Kyu Lee

Publisher 

Elsevier

Issue Date 

2008

Citation 

International Immunopharmacology, vol. 8, no. 7, pp. 967-973

Keywords 

(-)-syringaresinolapoptosisbaxBcl-2caspase-3CdkCdkisyringaresinolcell cycle arrest

Abstract 

We examined the effect of (-)-syringaresinol, a furofuran-type lignan isolated from Daphne genkwa, on cell cycle regulation in HL-60 human promyelocytic leukemia cells in vitro. (-)-Syringaresinol decreased the viability of HL-60 cells by inducing G1 arrest followed by apoptosis in a dose- and time-dependent manner. The G0/G1 phase of the cell cycle is regulated by cyclin-dependent kinases (Cdk), cyclins and cyclin-dependent kinase inhibitors (Cdki). We show by western blot analysis, that the (-)-syringaresinol-induced G1 arrest was mediated through the increased expression of Cdki proteins (p21cip1/waf1 and p27kip1) with a simultaneous decrease in cdk2, cdk4, cdk6, cyclin D1, cyclin D2, and cyclin E expression. The induction of apoptosis after treatment with (-)-syringaresinol for 24 h was demonstrated by morphological changes, DNA fragmentation, altered ratio of Bax/Bcl-2, cleavage of poly(ADP-ribose) polymerase and flow cytometry analysis. (-)-Syringaresinol also induced cytochrome c release and activation of caspase-3 and caspase-9. To our knowledge, this is the first time that (-)-syringaresinol has been reported to potently inhibit the proliferation of human promyelocytic HL-60 cells through G1 arrest and induction of apoptosis. These findings suggest that (-)-syringaresinol may be a potential chemotherapeutic agent for the treatment of cancer.

ISSN 

1567-5769

Link 

http://dx.doi.org/10.1016/j.intimp.2008.02.012

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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