Abstract: OBJECTIVE To explore the effects of micheliolide(MCL) on the proliferation and apoptosis of colon cancer cells and its potential mechanism. METHODS Azoxymethane(AOM)/dextran sodium sulfate(DSS) mouse colon cancer model was established by intraperitoneal injection of AOM and DSS. The mice were injected with cisplatin 2.5 mg·kg^-1, 0, 10, 20 and 50 mg·kg^-1 of MCL into the tail vein, respectively, and the survival rate was recorded for 30 d. Tumor tissues were taken and the tumors were weighed. Ki67 and caspase-3 protein expression levels in mouse tumor tissues were examined by immunohistochemistry, and PTEN protein expression in mouse tumor tissues was detected by Western blotting. Colon cancer cell line SW620 was cultured in medium containing cisplatin 10 µmol·L^-1, MCL 0, 2.5, 5, 10 µmol·L^-1, or transfected with siPTEN in MCL 0 and 10 µmol·L^-1, respectively. Cell proliferation was detected by BrdU cell proliferation assay, apoptosis was detected by flow cytometry, and cell proliferation antigen(Ki67, PCNA), apoptosis-related protein(cleaved caspase-3, Bcl-2, Bax) and PTEN protein expression were detected by Western blotting. RESULTS Compared with the model group, MCL increased the survival rate of mice, reduced tumor weight, increased tumor inhibition rate, up-regulated PTEN protein expression, decreased Ki67 positive cells, and increased caspase-3 positive cells(P<0.05 or P<0.01). Compared with the control group, MCL decreased the percentage of BrdU-positive cells, down-regulated the expression of Ki67 and PCNA, increased the apoptosis rate, down-regulated the expression of Bcl-2, and up-regulated the expression of Bax, cleaved caspase-3 and PTEN in colon cancer cells(P<0.05 or P<0.01). Inhibition of PTEN expression could reverse the effects of costunolide on SW620 cell proliferation and apoptosis(P<0.01). CONCLUSION MCL inhibits the proliferation and induces apoptosis of colorectal cancer cells, which is related to the up-regulation of PTEN expression.