G2 cell cycle arrest and apoptosis are induced in Burkitt's lymphoma cells by the anticancer agent oracin
- 2 January 1997
- journal article
- Published by Wiley in FEBS Letters
- Vol. 400 (1), 127-130
- https://doi.org/10.1016/s0014-5793(96)01307-5
Abstract
The cytotoxic effect of the new potential intercalating anticancer drug oracin was studied on Burkitt's lymphoma cell line that overexpressed bcl‐2 (BL bcl‐2) and a control transfectant without the bcl‐2 gene (BL SV2). Oracin showed a marked cytostatic effect on both BL SV2 and BL bcl‐2 cells. IC50, as measured by the MTT assay, was approx. 5‐times greater for BL bcl‐2 cells (5.0 μmol/l) than for BL SV2 cells (1.0 μmol/l). There was no significant increase in apoptosis after 24 h of treatment with oracin (1.0 μmol/l) in both cell lines. However, after 48 h from the removal of oracin in BL SV2 culture the levels of apoptotic and secondary necrotic cells increased to 20 and 37%, respectively. In contrast, BL bcl‐2 cells treated in a similar manner showed only basal levels of apoptotic and secondary necrotic cells. Analysis of the cell cycle profiles showed a significant increase of S and G2/M phases of the cell cycle in both cell lines after 6 h of drug treatment (1.0 μmol/l). The cells were arrested in G2/M phase of the cell cycle after 24 h, with no significant changes in cell viability. After 72 h, the viable BL SV2 cells were still in G2/M, however, the viability of this culture had fallen to approx. 5%. Flow cytometry analysis of the DNA content revealed the presence of a ‘sub‐G2’ region, which represented the apoptotic cells. The BL SV2 cells died after 72 h while they were in the G2/M phase. Although the treated BL bcl‐2 cells were similarly arrested in the G2/M phase, they nevertheless remained with a relatively high viability (68%).Keywords
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