AIM:To investigate the inhibitory effect of ubiquitin-proteasome pathway(UPP)on proliferation of esophagealcarcinoma cells.METHODS:Esophageal carcinoma cell strain EC9706 wastreated with MG-132 to inhibit its UPP specificity.Cell growthsuppression was evaluated with 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide(MTT)assay.DNAsynthesis was evaluated by ~3H-thymidine(~3H-TdR)incorporation.Morphologic changes of cells were observedunder microscope.Activity of telomerase was examinedby telomeric repeat amplification protocol(TRAP)of PCR-ELISA.Cell cycle and apoptosis were detected by flowcytometry(FCM).DNA fragment analysis was used toconfirm the presence of apoptosis.Expression of p27~(kip1)was detected by immunocytochemical technique.RESULTS:After exposed to MG-132,the growth and valueof ~3H-TdR incorporation of EC9706 cells were obviouslyinhibited.Cells became round,small and exfoliative undermicroscope.TRAP PCR-ELISA showed that light absorptionof cells gradually decreased after exposed to 5μmol/L ofMG-132 for 24,48,72 and 96 h(P<0.01).The percentageof cells at G_0/G_1 phase was increased and that at S andG_2/M was decreased(P<0.01).The rate of apoptotic cellstreated with 5 μmol/L of MG-132 for 48 and 96 h was 31.7%and 66.4%,respectively.Agarose electrophoresis showedmarked ladders.In addition,the positive signals of p27~(kip1)were located in cytoplasm and nuclei in MG-132 group incontrast to cytoplasm staining in control group.CONCLUSION:MG-132 can obviously inhibit proliferationof EC9706 cells and induce apoptosis.The mechanismsinclude upregulation of p27~(kip1) expression,G_1 arrest anddepression of telomerase activity.The results indicate thatinhibiting UPP is a novel strategy for esophageal carcinomatherapy. AIM: To investigate the inhibitory effect of ubiquitin-proteasome pathway (UPP) on proliferation of esophagealcarcinoma cells. METHODS: Esophageal carcinoma cell strain EC9706 wastreated with MG- 132 to inhibit its UPP specificity. Cell growth suppression was evaluated as 3- (4,5 -dimethylthiazole-2-yl) -2,5-diphenyl tetrazolium bromide (MTT) assay. DNA synthesis was performed by ~ 3H-thymidine (~ 3H- TdR) incorporation. Mosaicologic changes of cells were observed in microscope. Activity of telomerase was examined by telomeric repeat amplification protocol (TRAP) of PCR-ELISA. Cell cycle and apoptosis were detected by flowcytometry (FCM). DNA fragment analysis was used toconfirm the presence of apoptosis. Expression of p27 ~ (kip1) was detected by immunocytochemical technique. exposed to MG-132, the growth and value of ~ 3H-TdR incorporation of EC9706 cells were obviously inhibited. Cells became round, small and exfoliative undermicroscope. TRAP PCR-ELISA showed that light absorption of cells gradually decrea The percentage of cells at G_0 / G_1 phase was increased and that at S and G2 / M was decreased (P <0.01). The rate of apoptotic cellstreated with 5 μmol / L of MG-132 for 48 and 96 h was 31.7% and 66.4%, respectively.Agarose electrophoresis showed markedly ladders. In addition, the positive signals of p27 ~ (kip1) were located in cytoplasm and nuclei in MG-132 group incontrast to cytoplasm staining in control group. CONCLUSION: MG-132 can demonstrably inhibit proliferation of EC9706 cells and induce apoptosis. The mechanisms include upregulation of p27 ~ (kip1) expression, G_1 arrest and depression of telomerase activity. thatinhibiting UPP is a novel strategy for esophageal carcinomatherapy.