Effect of realgar on expression of survivin in leukemia cell lines and its significance

To study the effect of realgar on expression of survivin in leukemia cell lines, HL-60 and Jurket cell lines were used as in vitro models. The expression of survivin was detected by Western blot analysis and immunofluorescence, and the expressions of Fas and caspase-3 were examined by immunohistoche...

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Published inZhongguo shi yan xue ye xue za zhi Vol. 13; no. 3; p. 386
Main Authors Xiao, Yan-Feng, Liu, Ya, Liu, Shan-Xi, Ren, Li-Fen
Format Journal Article
LanguageChinese
Published China 01.06.2005
Subjects
Antineoplastic Agents - pharmacology
Apoptosis - drug effects
Arsenicals - pharmacology
Blotting, Western
Caspase 3 - metabolism
Dose-Response Relationship, Drug
fas Receptor - metabolism
Fluorescent Antibody Technique
HL-60 Cells
Humans
Immunohistochemistry
Inhibitor of Apoptosis Proteins
Jurkat Cells
Leukemia - metabolism
Leukemia - pathology
Microtubule-Associated Proteins - biosynthesis
Neoplasm Proteins - biosynthesis
Sulfides - pharmacology
Time Factors
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Summary:To study the effect of realgar on expression of survivin in leukemia cell lines, HL-60 and Jurket cell lines were used as in vitro models. The expression of survivin was detected by Western blot analysis and immunofluorescence, and the expressions of Fas and caspase-3 were examined by immunohistochemistry. The results showed that the expression of survivin was positive in the two cell lines. HL-60 cells did not express Fas and caspase-3, and Jurket cells were Fas-positive and caspase-3 was negative. Realgar induced a dose- and time-dependent down-regulation of survivin expression in Jurket cells, and especially in HL-60. Caspase-3 expression changed from negative to positive in HL-60 cell, but there still was no expression in Jurket cell. It is concluded that survivin expression level decreased during leukemia cell apoptosis induced by Realgar. The down-regulation of survivin expression may be an important mechanism in leukemia cell apoptosis induced by realgar through mitochondrial pathway.
ISSN:1009-2137