1997Chinese Journal of Cancer ResearchRequires access

Induction of apoptosis of human leukemia cells by α-anordrin

Liguang Lou, Bin Xu

Open publisher page 3 citations

Abstract

The apoptosis-inducing effect of α-anordrin (ANO) was investigated in this study. ANO 10–50 µM inhibited the growth of both human leukemia HL-60 and K562 cells by 19–52%. Electron microscopy showed that ANO-treated cells exhibited the drastic changes including cell shrinkage, chromatin condensation, nuclear fragmentation, typical of apoptosis. Gel electrophoresis of DNA extracted from both HL-60 and K562 cells treated with ANO revealed characteristic “ladder” pattern. ANO 50 µM for 48 h caused approximately 50–70% apoptosis. Cycloheximide (CHX) and actinomycin D (Act D) did not prevent ANO-induced apoptosis in K562 cells, however, apoptosis of HL-60 cells in the presence of ANO was partially blocked by these two agents. Moreover, it was found that tamoxifen synergically potentiated and estradiol partially antagonized ANO-induced apoptosis in HL-60 cells. Results demonstrated that ANO could induce tumor cell apoptosis, which might contribute to its anticancer action.

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What this paper is about

The apoptosis-inducing effect of α-anordrin (ANO) was investigated in this study. ANO 10–50 µM inhibited the growth of both human leukemia HL-60 and K562 cells by 19–52%. Electron microscopy showed that ANO-treated cells exhibited the drastic changes including cell shrinkage, chromatin condensation, nuclear fragmentation, typical of apoptosis. Gel electrophoresis of DNA extracted from both HL-60 and K562 cells treated with ANO revealed characteristic “ladder” pattern. ANO 50 µM for 48 h caused approximately 50–70% apoptosis. Cycloheximide (CHX) and actinomycin D (Act D) did not prevent ANO-induced apoptosis in K562 cells, however, apoptosis of HL-60 cells in the presence of ANO was partially blocked by these two agents. Moreover, it was found that tamoxifen synergically potentiated and estradiol partially antagonized ANO-induced apoptosis in HL-60 cells. Results demonstrated that ANO could induce tumor cell apoptosis, which might contribute to its anticancer action.

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Available abstract

The apoptosis-inducing effect of α-anordrin (ANO) was investigated in this study. ANO 10–50 µM inhibited the growth of both human leukemia HL-60 and K562 cells by 19–52%. Electron microscopy showed that ANO-treated cells exhibited the drastic changes including cell shrinkage, chromatin condensation, nuclear fragmentation, typical of apoptosis. Gel electrophoresis of DNA extracted from both HL-60 and K562 cells treated with ANO revealed characteristic “ladder” pattern. ANO 50 µM for 48 h caused approximately 50–70% apoptosis. Cycloheximide (CHX) and actinomycin D (Act D) did not prevent ANO-induced apoptosis in K562 cells, however, apoptosis of HL-60 cells in the presence of ANO was partially blocked by these two agents. Moreover, it was found that tamoxifen synergically potentiated and estradiol partially antagonized ANO-induced apoptosis in HL-60 cells. Results demonstrated that ANO could induce tumor cell apoptosis, which might contribute to its anticancer action.

Key concepts: Apoptosis, K562 cells, DNA fragmentation, Leukemia, Molecular biology, Cycloheximide, Fragmentation (computing), Chemistry

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