Emodin Induces Leukemic HL-60 Cells Apoptosis by Inhibiting PI3K/Akt Signal Pathway.

Abstract Emodin (1.3.8-trihydroxy-6-methylanthraquinone), a traditional Chinese herbal medicine, which is a natural anthraquinone compound from the root and rhizome of Rheum palmatum, has been shown to display a number of biological activities such as antiviral, antimicrobial, immunosuppressive, anti-inflammatory, and anticancer. Recent studies showed that it can inhibit proliferation of multiple cancer cells such as breast, hepatocellular, and lung cancer cells in vitro. The PI3K signal transduction pathway has been investigated extensively for its role in oncogenic transformation and in the prevention of apoptosis. The aim of the present study was to investigate the effects of Emodin on inhibiting cell growth and inducing apoptosis in human myeloid leukemia cell line HL-60, and to examine how emodin affects the PI3K/AKT signalling pathway, leading to cell apoptosis. HL-60 cells were exposed to various dosages of Emodin. MTT assay was used to detect HL-60 cell proliferation. Distribution of HL-60 cells in cell cycle was analyzed by flow cytometry and cell apoptosis was observed by MitoCapture apoptosis detection. The protein expressions of Akt signal pathway were detected by Western-Blot. The results showed that Emodin remarkably inhibited the cell proliferation, with 20μmol/L of the IC50 value for 48h. Apoptosis in HL-60 cells could be efficiently induced by Emodin in a dose dependent manner and cells were arrested at G0/G1. The expressions of Akt,p-Akt,IκB-α,p-IκB-α,p65,p-p65,mTOR and p-mTOR in PI3K/Akt signal pathway were downregulated after Emodin treatment. It could be concluded that Emodin can efficiently induce growth inhibition and apoptosis in HL-60 cells .Akt signal pathway may be involved in this process.