AIM:To examine whether and how rosiglitazone enhances apoptosis induced by fluorouracil in human colon cancer(HT-29)cells.METHODS:Human colon cancer HT-29 cells were cultured in vitro and treated with fluorouracil and/or rosiglitazone.Proliferation and growth of HT-29 cells were evaluated by MTT assay and trypan blue exclusion methods,respectively.The apoptosis of HT-29 cells was determined by acridine orange/ethidium bromide staining and flow cytometry using PI fluorescence staining.The expressions of peroxisome proliferator-activated receptor γ(PPARγ),Bcl-2 and Bax in HT-29 cells were analyzed by Western blot.RESULTS:Although rosiglitazone at the concentration below 30 μmol/L for 72 h exerted almost no inhibitory effect on proliferation and growth of HT-29 cells,it could significantly enhance fluorouracil-induced HT-29 cell proliferation and growth inhibition.Furthermore,10 μmol/L rosilitazone did not induce apoptosis of HT-29 cells but dramatically enhanced fluorouracil-induced apoptosis of HT-29 cells.However,rosiglitazone did not improve apoptosis induced by fluorouracil in HT-29 cells pretreated with GW9662,a PPARγ antagonist.Meanwhile,the expression of Bax and PPARγ was up-regulated,while the expression of Bcl-2 was down regulated in HT-29 cells treated with rosiglitazone in a time-dependent manner.However,the effect of rosiglitazone on Bcl-2 and Bax was blocked or diminished in the presence of GW9662.CONCLUSION:Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating PPARγ. AIM: To examine whether and how rosiglitazone enhances apoptosis induced by fluorouracil in human colon cancer (HT-29) cells. METHODS: Human colon cancer HT-29 cells were cultured in vitro and treated with fluorouracil and / or rosiglitazone. Proliferation and growth of HT-29 cells were evaluated by MTT assay and trypan blue exclusion methods, respectively. The apoptosis of HT-29 cells was determined by acridine orange / ethidium bromide staining and flow cytometry using PI fluorescence staining. The expressions of peroxisome proliferator-activated receptor γ (PPARγ), Bcl-2 and Bax in HT-29 cells were analyzed by Western blot .RESULTS: Although rosiglitazone at the concentration below 30 μmol / L for 72 h exerted almost no inhibitory effect on proliferation and growth of HT-29 cells, it could significantly enhance fluorouracil-induced HT-29 cell proliferation and growth inhibition. Future Thermo, 10 μmol / L rosilitazone did not induce apoptosis of HT-29 cells but dramatically enhanced fluorouracil-induced apoptosis of HT-29 cells. Despite, rosiglitazone did not improve apoptosis induced by fluorouracil in HT-29 cells pretreated with GW9662, a PPARγ antagonist. Meanwhile, the expression of Bax and PPARγ was up-regulated, while the expression of Bcl- 2 was down regulated in HT-29 cells treated with rosiglitazone in a time-dependent manner. However, the effect of rosiglitazone on Bcl-2 and Bax was blocked or diminished in the presence of GW9662.CONCLUSION: Rosiglitazone enhances fluorouracil-induced apoptosis of HT -29 cells by activating PPARγ.