Background The treatment of patients with small cell lung cancer (SCLC) is based on chemotherapy.However,thetreatment is limited by the development of drug resistance.Emodin has been shown to exhibit an anti-cancer effect.Butthe molecular mechanism remains unclear.This study was conducted to investigate the effect of emodin on the geneexpression profile changes in SCLC NCI-H446 cells.Methods NCI-H446 cells were treated with emodin and cell viability was determined by MIT assay.Cell apoptosis wasdetermined by both flow cytometry and caspase-3 activity assay.The effect of emodin on the gene expression profile ofNCI-H446 cells was analyzed using cDNA microarray.Semi-quantitative reverse transcriptase-polymerase chain reaction(RT-PCR) was used to validate the microarray results.Results Emodin suppressed viability,induced apoptosis and changed cell cycle of NCI-H446 cells.Among the 1262genes,10 genes were up-regulated and 8 genes were down-regulated more than 2 folds in NCI-H446 cells whencompared with the control cells after treatment with emodin for 12 hours,while 12 genes were up-regulated and 24 geneswere down-regulated after treatment with emodin for 24 hours.These genes were involved in metabolism,signaltransduction,transcription regulation,cytoskeleton organization,immune response,transport,protein synthesis,cellcycle control,cell adhesion and RNA processing.The RT-PCR results were consistent with those obtained by themicroarray.Conclusions Emodin affects the expression of genes involved in various cellular functions and plays important roles incell apoptosis,tumor metastasis and chemotherapy-resistance,which suggests emodin might become an effectivechemopreventive or chemotherapeutic agent for SCLC.Chin Med J 2007;120(19):1710-1715 Background The treatment of patients with small cell lung cancer (SCLC) is based on chemotherapy. However, the treatment is limited by the development of drug resistance. Emodin has been shown to exhibit an anti-cancer effect. But the molecular mechanism remains unclear. This study was conducted to investigate the effect of emodin on the geneexpression profile changes in SCLC NCI-H446 cells. Methods NCI-H446 cells were treated with emodin and cell viability was determined by MIT assay. Cell apoptosis was determined by both flow cytometry and caspase-3 activity assay. The effect of emodin on the gene expression profile of NCI-H446 cells was analyzed using cDNA microarray. Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was used to validate the microarray results. Results Emodin suppressed viability, induced apoptosis and changed cell cycle of NCI-H446 cells. Among the 1262genes, 10 genes were up-regulated and 8 genes were down-regulated more than 2 folds in NCI-H446 cells whenc ompared with the control cells after treatment with emodin for 12 hours, while 12 genes were up-regulated and 24 genes were down-regulated after treatment with emodin for 24 hours. The genes are involved in metabolism, signal transduction, transcription regulation, cytoskeleton organization, immune response, transport, protein synthesis, cell cycle control, cell adhesion and RNA processing. The RT-PCR results were consistent with those obtained by themicroarray. Conclusions Emodin affects the expression of genes involved in various cellular functions and plays important roles in cell apoptosis, tumor metastasis and chemotherapy-resistance, which suggests emodin might become an effective chemopreventive or chemotherapeutic agent for SCLC. Chin Med J 2007; 120 (19): 1710-1715