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Objective: To investigate the roles of Bcl-xl and Bcl-xs in the development and progression of endometrial carcinoma, and to explore their correlation.Methods: The expression of Bcl-xl and Bcl-xs in 32 cases of endometrial carci-noma, 12 cases of endometrial atypical hyperplasia, 6 cases of endometrial simple hyperplasia and 10 cases of normal en-dometrial tissues were examined by RT-PCR and Western-blot.Results: The expression of Bcl-xl mRNA and protein was significantly higher in endometrial cancer tissues than in normal endometrial tissues (P<0.05), and was statistically associat-ed with the pathological stage of endometrial carcinoma.(F=5.33, P=0.02).The expression of Bcl-xs mRNA and protein in atypical endometrial hyperplasia and endometrial carcinoma tissues were significantlly lower than that in normal endometri-al tissues (P<0.05), which was also associated with clinical stage and lymph node metastasis of endometrial carcinoma (P<0.05).The expression of Bcl-xl was negatively correlated with the expression of Bcl-xs in different endometrial tissues (r=-0.76).Conclusion: The abnormal expression of Bcl-xs and Bcl-xl was a factor for the pathogenesis and development of endometrial carcinoma.The negative correlation between Bcl-xl and Bcl-xs in different endometrial tissues as well as their relative expression ratio may have certain impact on the genesis of endornetrial cancer.
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Objective To analyze the effect and mechanism of trichostatin A（TSA）on cell cycle in human ovarian cancer cells.Methods Human ovarian cancer cell line A2780 cells were cultured in RPMI 1640 supplement.Flow cytometry analysis and RT-PCR were used to examine the distribution of cell cycles and the level of p21WAF/CIPI mRNA.Results TSA induced increase of G2/M cells increased after the treatment of TSA for 36 hours（P 0.05）;the level of p21WAF/CIPI mRNA expression was upregulated after TSA treatment for 12 hours,the highest leve of its expression occurred at 24 hours,the expression level begun to decrease at 48 hours（P 0.05）.TSA simultaneously induced the decrease of S phase cells in a concentration-dependent manne（rP 0.05）.TSA upregulated the expression of p21WAF/CIPI mRNA in a concentration-dependent manner（P 0.05）.Conclusion TSA could block the G2/M phase and inhibits cell proliferation of A2780 cells through upregulating the expression of p21WAF/CIPI mRNA and the activate cyclin-dependent kinase.
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Objective To assess the effects of aspirin on the proliferation and apoptosis of human endometrial adenocarcinoma cells.Methods MTT assay was used to measure the effects of aspirin on the proliferation of Ishikawa cell.Flow cytometry(FCM) was employed to examine the distribution of cell cycles and the rates of apoptosis.Transmission electron microscopy was used to observe cell morphologic changes after aspirin administration.Results Aspirin inhibited the proliferation of cultured Ishikawa cells in a time-dependent and dose dependent manner(P<0.05).Aspirin increased the distribution of G,stage and the rates of cell apoptosis in a dose-dependent manner(P<0.05).Morphologic features of apoptosis cells,including cell shrinkage,nuclear condensation and apoptotic bodies could be found obviouslyunder the transmission electron microscopy.Conclusion Aspirin inhibited the proliferation and increased the apoptosis of human endometrial adenocarcinoma Ishikawa cells.
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OBJECTIVE: : To investigate the effect of aspirin on human Ishikawa adenocarcinoma endometrium cell proliferation and apoptosis and its related mechanism through in vitro experiments. METHODS: : The effects on Ishikawa adenocarcinoma endometrium cell proliferation and cell cycle of aspirin at different intervals and concentrations were determined with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide method and flow cytometry; cell morphous change after the effect of aspirin was observed with transmission electron microscope; and the effect of aspirin on B-cell lymphoma/leukemia-x, long (Bcl-xl) proteinum expression was determined with Western blot. RESULTS: : Aspirin had a significant depressant effect on human Ishikawa adenocarcinoma endometrium cell proliferation, and the effect showed time and dose dependence (P < 0.05). Aspirin-induced cell blockage at G1 phase, elevated cell apoptosis rate, and its effect were related with its concentration (P < 0.05). After treatment, cell volume was reduced, chromatin was seen concentrated and aggregated around the edge of nuclear membrane, and apoptotic body was formed. Aspirin decreased Bcl-xl proteinum expression, and the effect was related with its concentration (P < 0.05). CONCLUSIONS: : Aspirin has a distinct depressant effect on human Ishikawa adenocarcinoma endometrium cell growth, and its effect may be realized by lowering Bcl-xl proteinum expression.
