DMU-212 has been shown to evoke a mitochondrial apoptotic pathway in transformed fibroblasts and
breast cancer. However, recently published data indicated the ability of
DMU-212 to evoke apoptosis in both mitochondria- and receptor-mediated manner in two
ovarian cancer cell lines, namely A-2780 and SKOV-3, which showed varied sensitivity to the compound tested. The pronounced cytotoxic effects of
DMU-212 observed in A-2780 cells were related to the execution of extracellular apoptosis pathway and cell cycle arrest in G2/M phase. In view of the great anticancer potential of
DMU-212 against A-2780 cell line, the aim of the current study was to assess antiproliferative activity of
DMU-212 in xenograft model of
ovarian cancer. To evaluate in vitro metabolic properties of cells that were to be injected into SCID mice, uptake and decline of
DMU-212 in A-2780
ovarian cancer cell line was investigated. It was found that the concentration of the test compound in A-2780 cells was growing within first eight hours, and then the gradual decline was observed. A-2780 cells stably transfected with pcDNA3.1/Zeo(-)-Luc vector were subcutaneously inoculated into the right flanks of SCID mice. After seven days of the treatment with
DMU-212 (50mg/kg b.w),
tumor growth appeared to be suppressed in the animals treated with the compound tested. At day 14 of the experiment,
tumor burden in mice treated with
DMU-212 was significantly lower, as compared to untreated controls. Our findings suggest that
DMU-212 might be considered as a potential
anticancer agent used in
ovarian cancer therapy.