| Object: To investigate the anti-tumor effects of Virosecurinine on proliferation inhibition and apoptosis induction in human chronic myeloid leukemia K562 cells and explore the underlying mechanisms.Materials and methods: K562 cells were treated with Virosecurinine of different concentrations(6.25, 12.5, 25, 50, 100, 200 μmol/L) for 24, 48 and 72 h. CCK-8 method was used to detect the antitumor effect of K562 under in vitro condition. Inverted microscope was used to observe K562 cells treated with Virosecurinine morphological changes.The flow cytometry was used to observe the apoptotic ratio and cell cycle induced with the Virosecurinine in K562 cells. Light and Electron microscopy was used to observe morphological changes in the K562 cells treated with Virosecurinine. The m RNA levels of m TOR, SHIP-2, PTEN and BCR/ABL were detected using real-time RT-PCR pre and post-treatment of Virosecurinine.Results: The generation depression effects of K562 cells cultured in vitro were detected by CCK-8 technology and there were dose-time dependent relationships. The IC50 was 32.984 μmol/L at 48 h. The morphology of cells become small and round,the process of cell division got less were observed. The result of FCM technology indicated that the group with Virosecurinine concentrations in 6.25, 25 and 50 μmol/L can increase the apoptosis rate of K562, and the G1/S phase was retarded. Numerous autophagic vacuoles and apoptotic bodies were observed in K562 cells treated with 25 μmol/L Virosecurinine for 48 h by electron microscopy,the process of cell division got less were observed.The result of realtime-PCR indicated that Virosecurinine up-regulated the PTEN gene expression and down-regulated the m TOR, SHIP-2 and BCR/ABL expression in K562.Conclusion: Virosecurinine can inhibit growth and proliferation of the K562 cell lines.Virosecurinine induced apoptosis in K562 cells by affecting the expression of m TOR, SHIP-2, BCR/ABL and PTEN. |
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