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α anordrin induced apoptosis of leukemia K562 cells is not prevented by actinomycin D

Lou Li

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Abstract

AIM: To investigate the effect of actinomycin D (Act D) on the apoptosis induced by α anordrin (ANO) in human leukemia K562 cells. METHODS: Morphological changes were observed with light microscope; DNA content was measured by flow cytometry and DNA fragmentation analyzed by agarose gel electrophoresis. RESULTS: Exposure of K562 cells to ANO 50 μmol·L -1 for 24 h resulted in 10% cell apoptosis. RNA synthesis inhibitor, Act D 0 005 μmol·L -1 did not suppress ANO induced apoptosis. On the contrary, Act D augmented induction of apoptosis by ANO, causing an increase in apoptosis from 10% to 20%. Act D 0 5 μmol·L -1 itself induced 32% apoptosis of K562 cells. Cells in S phase were more sensitive to apoptosis in the presense of ANO, whereas Act D preferentially stimulated S and G 2 M Phase cells to undergo apoptosis. CONCLUSIONS: ANO induced apoptosis was not dependent on the synthesis of de novo RNA.

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What this paper is about

AIM: To investigate the effect of actinomycin D (Act D) on the apoptosis induced by α anordrin (ANO) in human leukemia K562 cells. METHODS: Morphological changes were observed with light microscope; DNA content was measured by flow cytometry and DNA fragmentation analyzed by agarose gel electrophoresis. RESULTS: Exposure of K562 cells to ANO 50 μmol·L -1 for 24 h resulted in 10% cell apoptosis. RNA synthesis inhibitor, Act D 0 005 μmol·L -1 did not suppress ANO induced apoptosis. On the contrary, Act D augmented induction of apoptosis by ANO, causing an increase in apoptosis from 10% to 20%. Act D 0 5 μmol·L -1 itself induced 32% apoptosis of K562 cells. Cells in S phase were more sensitive to apoptosis in the presense of ANO, whereas Act D preferentially stimulated S and G 2 M Phase cells to undergo apoptosis. CONCLUSIONS: ANO induced apoptosis was not dependent on the synthesis of de novo RNA.

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Available abstract

AIM: To investigate the effect of actinomycin D (Act D) on the apoptosis induced by α anordrin (ANO) in human leukemia K562 cells. METHODS: Morphological changes were observed with light microscope; DNA content was measured by flow cytometry and DNA fragmentation analyzed by agarose gel electrophoresis. RESULTS: Exposure of K562 cells to ANO 50 μmol·L -1 for 24 h resulted in 10% cell apoptosis. RNA synthesis inhibitor, Act D 0 005 μmol·L -1 did not suppress ANO induced apoptosis. On the contrary, Act D augmented induction of apoptosis by ANO, causing an increase in apoptosis from 10% to 20%. Act D 0 5 μmol·L -1 itself induced 32% apoptosis of K562 cells. Cells in S phase were more sensitive to apoptosis in the presense of ANO, whereas Act D preferentially stimulated S and G 2 M Phase cells to undergo apoptosis. CONCLUSIONS: ANO induced apoptosis was not dependent on the synthesis of de novo RNA.

Key concepts: Apoptosis, K562 cells, Agarose gel electrophoresis, DNA fragmentation, Molecular biology, Flow cytometry, Leukemia, Fragmentation (computing)

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