OBJECTIVE To investigate the anti-proliferative effect ofrosiglitazone and its relationship to peroxisome proliferator-activated receptor γ(PPARγ)in human breast cancer cell lineMDA-MB-231 and evaluate the potential application value ofrosiglitazone for breast cancer therapy.METHODS The cytostatic effect of rosiglitazone on MDA-MB-231 cells was measured by the MTT assay.Cell-cyclekinetics was assessed by flow cytometry.Apoptotic cells weredetermined by the TUNEL assay.MDA-MB-231 cells weretreated with rosiglitazone or in combination with the PPARγantagonist GW9662 to investigate the effect of rosiglitazone on cellproliferation and its relationship to PPARγ.RESULTS The results showed that rosiglitazone could inhibitgrowth of MDA-MB-231 cells in a dose- and time-dependentmanner with an IC_(50)value of 5.2μmol/L at 24 h after the drugwas added into the culture.Cell cycle analysis showed that thepercentage of G_0/G_1 phase cells increased,S phase cells decreased,and cells were arrested in G_1 phase with increasing concentrationsof rosiglitazone.Detectable signs of apoptotic cell death caused byrosiglitazone occurred at a concentration of 100 μmol/L and theapoptotic rate was (18±3)%.PPARγ selective antagonist GW9662could partially reverse the inhibitory effect of rosiglitazone onproliferation of MDA-MB-231 cells.CONCLUSION It was concluded that rosiglitazone can inhibitgrowth of MDA-MB-231 cells via PPARγ activation and a highconcentration of rosiglitazone can also induce MDA-MB-231 cellapoptosis.These results suggest that PPARγ represents a putativemolecular target for chemopreventive therapy and rosiglitazonemay be effective in the treatment of breast cancer. OBJECTIVE To investigate the anti-proliferative effect ofrosiglitazone and its relationship to peroxisome proliferator-activated receptor γ (PPARγ) in human breast cancer cell line MDA-MB-231 and evaluate the potential application value ofrosiglitazone for breast cancer therapy. METHODS The cytostatic effect of rosiglitazone on MDA-MB-231 cells was measured by the MTT assay. Cell-cycle assay was assessed by flow cytometry. Apoptotic cells were determined by the TUNEL assay. MDDA-MB-231 cells were treated with rosiglitazone or in combination with the PPAR gamma antagonist GW9662 to investigate the effect of rosiglitazone on cellproliferation and its relationship to PPARγ .RESULTS The results showed that rosiglitazone could inhibit growth of MDA-MB-231 cells in a dose- and time-dependent manne with an IC 50 (50) value of 5.2 μmol / L at 24 h after the drugwas added into the culture. Cell cycle analysis showed that the percentage of G_0 / G_1phase cells increased, S phase cells decreased, and cells were arreste d in G_1 phase with increasing concentrations of rosiglitazone. Detected signs of apoptotic cell death caused byrosiglitazone occurred at a concentration of 100 μmol / L and the apoptotic rate was (18 ± 3)%. PPARγ selective antagonist GW9662could partially reverse the inhibitory effect of rosiglitazone onproliferation of MDA-MB-231 cells. CONCLUSION It was caused that rosiglitazone can inhibit growth of MDA-MB-231 cells via PPARγ activation and a high concentration of rosiglitazone can also induce MDA-MB-231 cellellatosis. These results suggest that PPARγ represents a putativemolecular target for chemopreventive therapy and rosiglitazonemay be effective in the treatment of breast cancer.