NF-κB pathway is involved in griseofulvin-induced G2/M arrest and apoptosis in HL60 cells.

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Title:	NF-κB pathway is involved in griseofulvin-induced G2/M arrest and apoptosis in HL60 cells.
Authors:	林時宜 Yih-Huei Uen;Der-Zen Liu;Meng-Shih Weng;Yuan-Soon Ho;Shyr-Yi Lin
Contributors:	醫學系內科學科
Date:	2007
Issue Date:	2009-08-11 13:51:20 (UTC+8)
Abstract:	Griseofulvin (GF), an oral antifungal agent, has been shown to exert antitumorigenesis effect through G2/Mcell cycle arrest in colon cancer cells. But the underlying mechanisms remained obscure. The purpose of this study is to test the cytotoxic effect of GF on HL-60 and HT-29 cells and elucidate its underlying molecular pathways. Dosedependent and time-course studies byflowcytometry demonstrated that 30 to 60 mMGF significantly inducedG2/M arrest and to a less extend, apoptosis, in HL-60 cells. In contrast, only G2/M arrest was observed in HT-29 cells under similar condition. Pretreatment of 30 mM TPCK, a serine protease inhibitor, completely reversed GF-induced G2/M cell cycle arrest and apoptosis in HL-60 cells but not in HT-29 cells. The GF-induced G2/M arrest in HL-60 cells is reversible. Using EMSA and super-shift analysis, we demonstrated that GF stimulated NF-kB binding activity in HL-60 cells, which was completely inhibited by pretreatment of TPCK. Treatment of HL-60 with 30 mMGF activated JNK but not ERK or p38MAPK and subsequently resulted in phosporylation of Bcl-2. Pretreatment of TPCK to HL-60 cells blocked the GF-induced Bcl-2 phosphorylation but not JNK activation. Time course study demonstrated that activation of cdc-2 kinase activity by GF correlated with Bcl-2 phosphorylation. Taken together, our results suggest that activation of NF-kB pathway with cdc-2 activation and phosphorylation of Bcl-2 might be involved in G2/M cell cycle arrest in HL-60 cells. J. Cell. Biochem. 101: 1165–1175, 2007.
Relation:	Journal of Cellular Biochemistry.(101):1165-1175.
Data Type:	article
Appears in Collections:	[Department of Internal Medicine] Periodical Article

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