RESUMO
Objective:To explore the expressions of estrogen receptor α (ERα) and estrogen receptor β (ERβ) in Chinese female esophageal squamous cell carcinoma (ESCC) and their relationship with clinical pathological characteristics, marriage and childbearing factors and their prognostic impact.Methods:A total of 110 female patients with primary ESCC in Nanyang Center Hospital from January 2001 to December 2016 were selected. The expression levels of ERα and ERβ proteins were examined by immunohistochemistry (IHC). Logistic regression was used to analyze the correlations of ERα and ERβ expressions with marriage and childbearing factors (menstrual status, age of menarche, age of first birth and the number of pregnancy) and clinical pathological parameters (tumor location, tumor invasion depth, lymph node metastasis and tumor stage). Kaplan-Meier method was used for survival analysis and log-rank test was used. Cox proportional hazard model was used for survival multivariate analysis.Results:The expression rates of ERα and ERβ proteins were 37.3% (41/110) and 64.5% (71/110) in tissues of female ESCC patients, respectively. ERβ expression was closely correlated with tumor location ( χ2 = 0.999, P = 0.030), tumor stage ( χ2 = 11.097, P < 0.01) and the number of pregnancy ( χ2 = 6.304, P = 0.012). The number of pregnancy ( HR = 2.553, 95% CI 1.051-6.203, P = 0.039) and ERβ expression ( HR = 2.580, 95% CI 1.966-3.386, P < 0.01) were independent protective factors for the survival of patients. Furthermore, ERα expression ( HR = 0.530, 95% CI 0.384-0.739, P < 0.01) and lymph node metastasis ( HR = 0.663, 95% CI 0.512-0.858, P = 0.002) were independent risk factors for survival. Conclusion:ERα and ERβ expressions can predict the prognosis of female ESCC patients.
RESUMO
Objective To explore the effect of proliferation and apoptosis of Solanine on acute T lymphocyte leukemia (T-ALL) Jurkat cells and its mechanism.Methods After treated with different concentrations of Solanine,the proliferation of Jurkat cells was detected by CCK-8 assay,and the effect of Solanine on apoptosis of Jurkat cells were detected by flow cytometry.The expression of Bcl-2 and Bax in Jurkat cells were detected by Western blot,and the expression levels of Bcl-2 mRNA and Bax mRNA were detected by real-time fluorescence quantitative polymerase chain reaction.Results CCK-8 assay showed that Solanine significantly inhibited the proliferation of Jurkat cells in a dose-and time-dependent manner.The results of flow cytometry showed that the apoptosis rates of Jurkat cells treated with Solanine for 24 h were (2.40-± 0.98) ％,(28.43-± 4.86) ％,(41.56-± 1.87) ％,respectively,in a dose-dependent manner.Western blot showed that Solanine could increase the expression of Bax and decrease the expression of Bcl-2 in Jurkat cells,and they all were dose-dependent.Conclusion Solanine can significantly inhibit the proliferation and induce apoptosis of Jurkat cells.The mechanism is related to the up-regulation of Bax expression and down-regulation of Bcl-2 expression.
RESUMO
Objective To investigate the pathogen-related genes of atmospheric polluting disease so as to clarify the biology mechanism and provide the scientific basis.Methods By using the technique of dot blot hybridization,we analyzed genes’differential expression with cloning by exposure to ≥75 μg/m3 PM2.5 in heating season and < 75 μg/m3 PM2.5 in un-heating season in WI-38 human embryo lung cells.The levels of cytokines TNF-α,IL-2, IL-6 and IL-8 were determined by radio immunity assay. Results After 24h of treatment, compared with control group,more than 100μg/mL PM2.5 significantly increased TNF-α,IL-6 and IL-8 levels,and decreased IL-2 in WI-38 human embryo lung cells (P < 0.05 ).The clear stripe was found in 350 bp in 48 gene samples with segment with differential expression of genes exposed to different concentrations of PM2.5 in WI-38 human embryo lung cells.Through the dot blot hybridization,black brown spots were found in 41 samples in Tester cDNA hybridization,and no similar spots were found in all of the same samples in Driver cDNA hybridization. Conclusion PM2.5 exposure may induce the inflammatory damage of WI-38 human embryo lung cells.Obvious genetic damage was observed in those cells exposed to ≥75 μg/m3 PM2.5 in heating season.
RESUMO
FOX genes code transcription factors. FOXO3a,FOXM1,FOXP3 are members of FOX genes family,which are associated with leukemia. Phosphorylated FOXO3a which loses the function of suppressing leu-kemia is inactive. Phosphorylated FOXO3a expresses in leukemic cell cytoplasm. FOXM1 is an oncogenesis tran-scription factor. FOXM1 highly expresses in myeloid leukemic cells. Expression of FOXP3 in leukemic cells has diversity. FOXP3 mainly expresses in T cell leukemic cells. These genes abrrant expressions play a key role in leukemia pathogenesis,development,therapy,drug resistance and prognosis.
RESUMO
Objective To study the effect of tetramethylpyrazine injection on proliferation and apoptosis of human acute lymphoblastic leukemia (ALL) cell line Jurkat and the relevant molecular mechanisms.Methods Cells were treated with tetramethylpyrazine injection at various concentrations (0,0.25,0.50,0.75,1.00,1.25 and 1.50 mg/ml),CCK-8 method was used to detect the inhibition rates at 24,48 and 72 h.After cells were treated with different concentrations of tetramethylpyrazine injection (0,0.50,1.00 and 1.50 mg/ml) for 48 h,the cell cycle and apoptosis were detected by flow cytometry,and the Aurora-B and Survivin protein expression were analyzed by Western blot.Results Compared with the control group (cells without tetramethylpyrazine injection treatment),various concentrations of tetramethylpyrazine injection could effectively inhibit Jurkat cells proliferation in a time-and dose-dependent manner (P ＜ 0.05),and IC50 at 24 h,48 h and 72 h after treatment were (1.33±0.16),(0.91±0.10) and (0.67±0.11) mg/ml,respectively.After cells were treated with tetramethylpyrazine injection at different concentrations (0.5,1.0 and 1.5 mg/ml) for 48 h,the number of treated cells in G2/M phase was increased,but that in S phase was decreased,and the apoptosis rates were significantly higher than that of control group,with a dose dependence (P ＜ 0.05).The results of Western blot showed that the expression levels of Aurora-B and Survivin in treated cells were lower than that of control group,also with a dose dependence (P ＜ 0.05).Conclusions Tetramethylpyrazine injection can effectively inhibit proliferation and induce apoptosis of Jurkat cells in vitro,and its underlying mechanisms involve with down-regulation of the Aurora-B and Survivin protein expression.