Emodin Induces Leukemia Cell Lines K562/Adr,HL-60 Apoptosis By Inhibiting Akt Signal Pathway

【Objective】To investigate the effects of Emodin on proliferation inhibition and apoptosis induction in human multidrug resistant leukemia cell lines K562/Adr cells and the role of PI3K/Akt signal pathway in the apoptosis of K562/Adr,HL-60 induced by Emodin .【Methods】K562/Adr cell was exposed to various dosages of Emodin. MTT assay was used to detect K562/Adr cell proliferation. Apoptosis of K562/Adr cells induced by Emodin was examined by DNA fragmentation analysis,flow cytometry,and detection of TdT mediated dUTP nick end labeling(TUNEL). The protein expressions of c-myc,P210 and Akt signal pathway were detected by Western Blotting.【Results】(1)The results showed that Emodin could remarkably inhibit the K562/Adr cell proliferation, and the IC50 value at 72h of treatment was about 20μmol/L.Apoptosis in K562/Adr cells could be induced by Emodin in a dose dependent manner.(2)The expressions of c-myc,bcr/abl and mdr-1 mRNA and protein decreased in K562/Adr cells treated with Emodin. (3)The expression of Akt,p-Akt,IκB-α,p-IκB-α,p65,p-p65,mTOR and p-mTOR in Akt signal pathway of K562/Adr,HL-60 cells was downregulated after Emodin treatment.【Conclusion】(1)Emodin could efficiently inhibit cell growth and induce apoptosis in K562/Adr cells, in which down-regulation of c-myc,bcr/abl and mdr-1 expressions may involve.(2)Akt signal pathway may be involved in apoptosis of K562/Adr and HL-60 cells after treatment with Emodin.