Vitamin E succinate-induced apoptosis in drug-resistant leukemia K562/ADM cells

OBJECTIVE: To explore the apoptosis of K562/ADM cells induced by Vitamin E succinate(VES) and its possible molecular mechanisms. METHODS: The multidrug-resistant K562/ADM cells cultured in vitro acted as the target cells. The proliferation of K562/ADM cells were determined with an MTT colorimetric assay; Wright-Giemsa staining was used to examine morphological changes of apoptosis. The cell cycle was analyzed by using flow cytometry (FCM); DNA fragmentation was examined by agarose gel electrophoresis; expressing level of Fas, Bcl-2 and p53 protein was measured with FCM. RESULTS: VES significantly inhibited the proliferation of K562/ADM cells,P=0.004. Typical morphological changes of apoptosis were observed through light microscopy. Cell cycle analysis indicated increased Sub-G 1 proportion and apoptosis rate, as well as apparent G 1 phase arrest,P=0.005. DNA fragmentation was significantly showed via agarose gel electrophoresis. After application of VES, expression of Fas protein increased (P=0.002)and Bcl-2 protein decreased markedly (P=0.000), and no obvious change of expression was found in p53 protein expression.CONCLUSIONS:VES induces apoptosis in multidrug-resistant K562/ADM cells, and the up-regulation of Fas protein and the down-regulation of Bcl-2 protein may play important roles in VES-induced apoptosis of K562/ADM cells.