Induction of apoptosis of human leukemia cells by α-anordrin
Liguang Lou, Bin Xu
Abstract
Liguang Lou, Bin Xu
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.
OpenAlex reports 3 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
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