Aim. MI1 is a promising maleimide derivative, which exhibits antiproliferative effect on different cells. The aim of present study was to investigate influence of MI1 on the cell cycle of cancer cells and its cytotoxity. Methods. The proliferative activity and viability of human cancer cell lines (colorectal adenocarcinoma-Colo-205; breast cancer-MCF-7; cervix cancer HeLa) obtained with MTT-test and cell counts were performed using a tripan blue dye. Distribution of cell cycle phases was obtained using flow cytometry method. Results. In the present study we demonstrate a detectable cytostatic effect of the maleimide derivative MI1 on the epithelial cell lines Colo-205, MCF-7 and HeLa. In the presence of MI1 the number of cells in the G 2 /M+S phases of the cell cycle dropped by 20-30 % (p < 0.05) relative to control. Conclusions. The results suggest that MI1 may be a perspective drug for antitumor therapy and perhaps deserves further study in detail.

AimTo purify the platelet aggregation inhibitor from Echis multisquamatis snake venom (PAIEM) and characterize its effect on platelet aggregation and HeLa cell proliferation.MethodsSodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and matrix assisted laser desorption/ionization time-of-flight (MALDI-TOF) were used for PAIEM identification. Platelet aggregation in the presence of PAIEM was studied on aggregometer Solar-AP2110. The changes of shape and granularity of platelets in the presence of PAIEM were studied on flow cytometer COULTER EPICS XL, and degranulation of platelets was estimated using spectrofluorimetry. Indirect enzyme-linked immunosorbent assay was used for the determination of target of PAIEM on platelet surface. An assay based on 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide was used to evaluate the effect of PAIEM on the proliferation of HeLa cells in cell culture.ResultsThe molecular weight of the protein purified from Echis multisquamatis venom was 14.9 kDa. Half-maximal inhibitory concentration (IC50) of PAIEM needed to inhibit adenosine diphosphate (ADP)-induced platelet aggregation was 7 μM. PAIEM did not affect thrombin- or ADP-induced platelet activation, but it did prevent binding of the anti-IIb antibody to glycoprotein IIb/IIIa (GPIIbIIIa)-receptor of adhered platelets and inhibited the viability of HeLa cells by 54%.ConclusionAs a member of the disintegrin family, PAIEM inhibited platelet aggregation and cell proliferation possibly by blocking integrin-mediated interactions. However, it did not impair cellular signaling causing any changes in platelet shape and granularity and did not affect ADP-induced platelet degranulation. This disintegrin was shown to be a potent inhibitor of integrin-mediated cellular interactions including platelet aggregation or cancer cell proliferation.

The obtained results demonstrate that our compound can serve as a base for further structure optimization in order to design new high-effective antimetastatic and antitumor agents.

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