To gauge whether caspase 3 activation is involved in the apoptosis induced by peptidimer c in K562 cells, K562 cells were treated with 10 mM caspase inhibitor for 2 h followed by 0, 9, 18, and 27 mMof peptidimerc for another 6 h, and examined caspase 3 expression by FACS. The outcome showed that AG 879 the percentage of caspase 3 was considerably reduced, compared to those treated only with peptidimer d. These findings suggested that peptidimer d may possibly induce the apoptosis of K562 by causing the caspase 3 signaling. To elucidate the mechanism by which peptidimer c inhibits K562 cell proliferation and determine if cell growth inhibition concerned cell cycle modifications, flow cytometry analysis was completed to determine the alterations of cell cycle of K562 cells after treatment with various doses of peptidimer c or penetratin vector for 6 h. While the proportion of cells in S phase was 53, when cells were treated with peptidimer h. 09 _ 5. Three years before treatment, it plainly risen up to purchase Gemcitabine 89. 21 _ 6. 54% after 6 h treatment with 72 mM peptidimer c. Concomitantly, the percentage of cells in G0/G1 stage decreased from 25. 99 no 3. 16% in case of untreated cells to 0. 79 number 1. 37% for cells treatedwith 72 mMpeptidimer c. Thus, peptidimer d treatment for 6 h led to a significant increase of S phase cells clearly correlated with a decrease of G0/G1 phase cells in a concentration dependent manner. At while the penetratin vector therapy did not induce any change in G0/G1, S, and G2/M phases of cell cycle, the same time frame, the cell proportion in G2/M cycle slightly decreased. These results demonstrate that the changes in cell cycle progression are particularly because of peptidimer h and that the inhibition Eumycetoma of K562 cells proliferation proceeds via an S phase arrest. In order to compare these results with the result of Gleevec1 on cell cycle, FCM analysis was conducted to test the cell cycle progression of K562 cells treated with various doses of imatinib. After 6 h therapy by imatinib at 2. 5 mM, no influence on G0/G1, S, and G2/M stages was observed. Nevertheless, after 24 h treatment, imatinib demonstrably induced a arrest in K562 cells. Concomitantly, a decrease of cells either in S or G2/M phases was observed, indicating that imatinib induced K562 cell growth was mediated by G0/G1phase charge. As described above, peptidimer c showed inhibition of K562 cells in a system different from that of Gleevec. Cell cycle distribution of K562 cells treated with peptidimer c in various levels for 24 h was observed by flow cytometry, as well as the cell cycle distribution of K562 cells treated with 27 mM peptidimer c or 0, to verify this aspect. 375 mM Gleevec in various time. The results showed that peptidimer c however arrested price PF299804 K562 cells in S phase, however, many cells seemed to increase again.