請用此 Handle URI 來引用此文件: http://hdl.handle.net/11455/32780
標題: Allyl isothiocyanate triggers G2/M phase arrest and apoptosis in human brain malignant glioma GBM 8401 cells through a mitochondria-dependent pathway
作者: Chen, N.G.
鍾楊聰
Chen, K.T.
Lu, C.C.
Lan, Y.H.
Lai, C.H.
Chung, Y.T.
Yang, J.S.
Lin, Y.C.
林永昌
關鍵字: allyl isothiocyanate
human brain malignant glioma GBM 8401 cells
apoptosis
mitochondria
G2/M arrest
cancer-cells
in-vivo
cruciferous vegetables
hela-cells
ht29 cells
growth
cycle
inhibition
induction
death
期刊/報告no:: Oncology Reports, Volume 24, Issue 2, Page(s) 449-455.
摘要: Isothiocyanates (ITCs) are present as glucosinolates in various cruciferous vegetables. Allyl isothiocyanate (AITC) is one of the common naturally occurring isothiocyanates. Recent studies have shown that AITC significantly inhibited survival of leukemia HL-60, bladder cancer UM-UC-3 and colon cancer HT-29 cells in vitro. In this study, we demonstrate that AITC significantly decreased proliferation and viability of human brain malignant glioma GBM 8401 cells in a dose-dependent manner with IC(50) 9.25+/-0.69 mu M for 24 h-treatment. The analysis of cell cycle distribution also showed that AITC induced significantly G2/M arrest and sub-G1 phase (apoptotic population) in GBM 8401 cells. AITC markedly reduced the CDK1/cyclin B activity and protein levels by CDK1 activity assay and Western blot analysis. AITC-induced apoptotic cell death and this evidence was confirmed by morphological assessment and DAPI staining. Pretreatment with specific inhibitors of caspase-3 (Z-DEVE-FMK) and -9 (Z-LEHD-FMK) significantly reduced caspase-3 and -9 activity in GBM 8401 cells. Western blot analysis and colorimetric assays also displayed that AITC caused a time-dependent increase in cytosolic cytochrome c, pro-caspase-9, Apaf-1, AIF, Endo G and the stimulated caspase-9 and -3 activity. Our results suggest that AITC is a potent anti-human brain malignant glioma drug and it shows a remarkable action on cell cycle arrest before commitment for apoptosis is reached.
URI: http://hdl.handle.net/11455/32780
ISSN: 1021-335X
文章連結: http://dx.doi.org/10.3892/or_00000878
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