Figure 2
Leukemia cells show reduced mitotic arrest when decatenation is inhibited. (A) Normal human CD34+ hematopoietic progenitors, 697 ALL, and THP-1 AML cells were treated with 10 μM ICRF-193 for 24 hours and then evaluated for the increase in G2/M cell-cycle fraction by propidium iodide staining for DNA content. (B) Mitotic arrest was induced by 10 μM ICRF-193 for 18 hours in CD34+ cells, 697 ALL and REH ALL cells, and THP-1 and KG-1 AML cells. HEK-293T cells, which do not express Metnase, served as a positive control for mitotic arrest after Topo IIα decatenation inhibition. Metaphase cells were imaged by tubulin immunofluorescence and DAPI nuclear morphology and quantified as a percentage of the total cell population with DMSO control subtracted. (C) Mitotic arrest induced by 10 μM ICRF-193 for 4 or 24 hours in CD34+ cells, 697 ALL and REH ALL cells, and THP-1 and KG-1 AML cells. HEK-293T cells, which do not express Metnase, served as a positive control for mitotic arrest after Topo IIα decatenation inhibition. Cells in mitosis were imaged by MPM-2 immunofluorescence and quantified as a percentage of the total population with DMSO control subtracted. The acute leukemia cell lines all have decreased mitotic arrest after Topo IIα inhibition with ICRF-193 compared with CD34+ cells. All experiments represent the average of at least 3 independent experiments, ± SEM. *Student t test (P < .05); **Student t test (P < .01).

Leukemia cells show reduced mitotic arrest when decatenation is inhibited. (A) Normal human CD34+ hematopoietic progenitors, 697 ALL, and THP-1 AML cells were treated with 10 μM ICRF-193 for 24 hours and then evaluated for the increase in G2/M cell-cycle fraction by propidium iodide staining for DNA content. (B) Mitotic arrest was induced by 10 μM ICRF-193 for 18 hours in CD34+ cells, 697 ALL and REH ALL cells, and THP-1 and KG-1 AML cells. HEK-293T cells, which do not express Metnase, served as a positive control for mitotic arrest after Topo IIα decatenation inhibition. Metaphase cells were imaged by tubulin immunofluorescence and DAPI nuclear morphology and quantified as a percentage of the total cell population with DMSO control subtracted. (C) Mitotic arrest induced by 10 μM ICRF-193 for 4 or 24 hours in CD34+ cells, 697 ALL and REH ALL cells, and THP-1 and KG-1 AML cells. HEK-293T cells, which do not express Metnase, served as a positive control for mitotic arrest after Topo IIα decatenation inhibition. Cells in mitosis were imaged by MPM-2 immunofluorescence and quantified as a percentage of the total population with DMSO control subtracted. The acute leukemia cell lines all have decreased mitotic arrest after Topo IIα inhibition with ICRF-193 compared with CD34+ cells. All experiments represent the average of at least 3 independent experiments, ± SEM. *Student t test (P < .05); **Student t test (P < .01).

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