RESUMEN
According to the method used in our laboratory,our group synthesized (DIPP-Trp)2-Lys-OCH 3. It inhibited the proliferation of K562 and HeLa cells in a dose-and time-dependent manner with an IC 50 of 15.12 and 42.23 microM, respectively. (DIPP-Trp) 2-Lys-OCH3 induced a dose-dependent increase of the G2/M cell population in K562 cells, and S cell population in HeLa cells;the sub-G0 population increased dramatically in both cell lines as seen by PI staining experiments using a FACS Calibur Flow cytometer (BeckmanCoulter,USA). Phosphatidylserine could signi?cantly translocate to the surface of the membrane in (DIPP-Trp)2-Lys-OCH3-treated K562 and HeLa cells.The increase of an early apoptotic population was observed in a dose-dependent manner by both annexin-FITC and PI staining.It was concluded that (DIPP-Trp) 2-Lys-OCH3 not only induced cells to enter into apoptosis,but also affected the progress of the cell cycle.It may have arrested the K562 and HeLa cells in the G 2/M,S phases,respectively.The apoptotic pathway was pulsed at this point,resulting in the treated cells entering into programmed cell death.(DIPP- Trp)-Lys-OCH is a potential anticancer drug that intervenes in the signalling pathway.