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Effect of PI3K/Akt inhibitor wortmannin on proliferation and apoptosis of leukemia K562 cells
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Abstract:
Objective:To study the effect of wortmannin (WM), a PI3K/Akt inhibitor, on the proliferation and apoptosis of leukemia cells and the possible mechanism. Methods:Human leukemia cell line K562 was treated with different concentrations of WM. The proliferation of K562 cells was examined by MTT assay. DNA damage in K562 cells was examined by single cell gel electrophoresis assay, and apoptosis of K562 cells was detected by Annexin VFITC/PI doublestaining. The expressions of total Akt, phosphorateAkt (pAkt), and NFκB p65 mRNA and protein were detected by RTPCR and Western blotting, respectively. Results:WM inhibited the proliferation of K562 cells in a dose and timedependent manner, with the IC50 value of 24 h being 25 nmol/L. WM also induced apoptosis of K562 cells in a dosedependent manner. DNA damage in K562 cells was demonstrated by appearance of comet tail after treatment with WM, with the rate of DNA tail and the tail length being significantly higher than those in the control group (P<0.01). WM dosedependently inhibited PAkt and NFκB p65, but not the total Akt, mRNA and protein expressions. Conclusion:WM can inhibit proliferation and induce apoptosis of K562 cells in a dose and timedependent manner, probably through downregulation of phosphorate PI3K/Akt signal pathway and NFκB expression.
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Project supported by the Education Foundation of Hubei Province
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