Of sodium valproate on chronic myeloid leukemia K562 cell line proliferation and apoptosis of.docVIP

 PAGE \* MERGEFORMAT 13 Of sodium valproate on chronic myeloid leukemia K562 cell line proliferation and apoptosis of [Abstract] of sodium valproate (VPA) for chronic myeloid leukemia cell line (K562 cells) proliferation and its possible mechanism. [Methods] CCK-8 to detect the impact of drugs on cell growth; the use of drugs by flow cytometry after treatment of apoptosis and cell cycle. [Results] VPA on the growth of K562 cells in a concentration - time-dependent inhibition; also lead to increased apoptosis (11.47% ± 0.25%), and normal control group (4.77% ± 0.40%) the difference was statistically significant compared with (P amp;lt;0.05); G0/G1 phase cells increased (82.30% ± 9.41%), S phase cells decreased (12.88% ± 6.99%), cells were arrest in the G0/G1 phase (P amp;lt;0.05). [Conclusion] VPA to block K562 cells in G0/G1 phase and ultimately inhibit tumor cell proliferation and induced apoptosis. [Keywords:] valproate granulocyte apoptosis in leukemia K562 cells of sodium valproate (VPA) on the proliferation of chronic myeloid leukemia cell line K562, and to explore possible mechanisms. [Methods] K562 cells were treated with VPA. Cell proliferation was determined by CCK-8 assay. Cell apoptosis and cell cycle were analyzed by flow cytometry (FCM). [Results] VPA inhibited the proliferation of K562 cells in concentration-and time-dependent manners. The apoptosis rate was significantly higher in the cells treated with VPA than in untreated cells [(11.47% ± 0.25%) vs (4.77% ± 0.40%), P amp;lt;0.05]. After treatment of VPA, cell cycle was arrested obviously at G0/G1 phase (P amp;lt;0.05). [Conclusions] VPA could induce G0/G1 phase arrest, inhibit the proliferation and induce the apoptosis of K562 cells in vitro. Keywords:: sodium valproate; chronic myeloid leukemia; K562 cell; proliferation; apoptosis Recent studies found that histone deacetylase inhibitors (histone deacetylase inhibitors, HDACI) can induce a variety of tumor cell growth arrest, diff