Inhibiting effect of emodin on adriamycin-resistance of K562/ADM cell line

The aim of the study was to evaluate and explore the inhibition effect of emodin on the adriamycin-resistance in K562/ADM cell line. In this study, verapamil and adriamycin were used as positive drug and tool drug, respectively. Cell viability was measured by MTT. The effect of emodin combined with adriamycin on cell cycle and apoptosis was determined by flowcytometry. The protein expression of P-gp, Bcr-Abl and STAT5 was analyzed by Western blot. Emodin inducing conformational change of P-gp with UIC2 antibody was detected by FCM. The results showed that emodin dramatically enhanced the cytotoxic effect of adriamycin in a concentration-dependent manner. Emodin promoted cell cycle arrest in G₂/M phase and adriamycin-induced apoptosis. It down-regulated the protein expression levels of P-gp, Bcr-Abl and STAT5. The results of the UIC2 binding experiment showed that emodin may not be the substrate of P-gp. It could effectively inhibit adriamycin-resistance in vivo. The mechanism of emodin inhibiting drug-resistance of K562/ADM may be related to the decrease of P-gp, Bcr-Abl and STAT5 protein expression, instead of competitive inhibition of P-gp.