(-)-Syringaresinol inhibits proliferation of human promyelocytic HL-60 leukemia cells via G1 arrest and apoptosis
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- (-)-Syringaresinol inhibits proliferation of human promyelocytic HL-60 leukemia cells via G1 arrest and apoptosis
- Bo Young Park; Sei Ryang Oh; Kyung Seop Ahn; Ok Kyong Kwon; Hyeong Kyu Lee
- Bibliographic Citation
- International Immunopharmacology, vol. 8, no. 7, pp. 967-973
- Publication Year
- 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.
- (-)-syringaresinol; apoptosis; bax; Bcl-2; caspase-3; Cdk; Cdki
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- Ochang Branch Institute > 1. Journal Articles
Ochang Branch Institute > Natural Medicine Research Center > 1. Journal Articles
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