AIM： Esophageal squamous cell carcinoma is generally sensitive to chemoradiotherapy （CRT）, but some cases are not. Using a retrospective analysis, we aimed to identify the predictors of the response by esophageal s...AIM： Esophageal squamous cell carcinoma is generally sensitive to chemoradiotherapy （CRT）, but some cases are not. Using a retrospective analysis, we aimed to identify the predictors of the response by esophageal squamous cell carcinoma to definitive CRT. METHODS： The intensities of expression of p53, Ki67, Bci-2, Bax, olclin D1, VEGF, CDC25B, and metallothionein （MT） were evaluated immunohistochemically in the biopsy specimens obtained before CRT, and the intensities of their expression were tested for correlations with the clinical effects of CRT. RESULTS： The esophageal squamous cell carcinomas with negative p53, positive CDC25B, and negative MT expression were found to be significantly more sensitive to CRT. In addition, p53 positivity and CDC25B positivity respomd well to CRT. CONCLUSION： Esophageal squamous cell carcinomas with negative p53,positive CDC25B, and negative MT expressions respond well to CRT. Even with p53 positivity, if with CDC25B positivity, CRT can be expected. 2005 The WJG Press and Elsevier Inc. All rights reserved展开更多
The aim of this experiment was to investigate whether FSH could regulate the proliferation of calf Sertoli cells and the relationship with CDC25 B through Wnt/β-catenin signaling pathway. The experimental method was ...The aim of this experiment was to investigate whether FSH could regulate the proliferation of calf Sertoli cells and the relationship with CDC25 B through Wnt/β-catenin signaling pathway. The experimental method was to culture Sertoli cells with different concentrations of FSH(40, 80, 120 and 150 ng · mL) and to treat the cultured cells with XAV939(β-catenin inhibitor) and to detect the expression of CDC25 B, CDC2, C-MYC and β-catenin. The results of the experiment showed that FSH could promote the proliferation of cells and its effect was good at 80 ng · mLconcentration. FSH could promote the expression of CDC25 B, CDC2, C-MYC and β-catenin. The expression of C-MYC and β-catenin in group FSH+XAV939 was lower than that in group FSH. There was no difference in mRNA expression of CDC25 B in group FSH and group FSH+XAV939. The protein expression of CDC25 B in group FSH+XAV939 was lower than that in group FSH. The conclusion was that FSH could promote the proliferation of calf Sertoli cells through Wnt/β-catenin signaling pathway. CDC25 B was upregulated by FSH and CDC2 could promote the proliferation of calf Sertoli cells. The protein level of CDC25 B was affected by Wnt/β-catenin signaling pathway.展开更多
Objective： To learn the effect of allitridi on inducing mitotic arrest in human gastric cell line SGC-7901 and its possible mechanisms. Methods： We treated SGC-7901 cells with allitridi, and observed the proliferati...Objective： To learn the effect of allitridi on inducing mitotic arrest in human gastric cell line SGC-7901 and its possible mechanisms. Methods： We treated SGC-7901 cells with allitridi, and observed the proliferation inhibitory rate with MTT colometric assay, changes of cell cycle using flow cytometry and Switzerland-Giemsa＇s staining, and morphologic changes of the microtubule structure and location changes of cyclin BI expression using immunofluorescence and confocal laser scanning microscope. Furthermore, the expression of cyclin B1 was analyzed quantitatively using Leica confocal software. Results： SGC-7901 cells were inhibited after exposure to allitridi and the IC50 was 7.2μg/ml for 24 h, 20μg/ml for 72 h. When the cells were treated with allitridi at concentrations of 3, 6, and 9μg/ml for 24 h respectively, there was a declining tendency in the percentage of G0/G1 cell but an increasing tendency in GE/M cell in the allitridi treated group compared with that of control （P〈0.01）. When cells were treated allitridi at concentration of 6 μg/ml for 24 h, its mitotic index was much higher （P〈0.01） than that of control, suggesting that allitridi caused arrest of gastric cancer cells in M phase. The cells were treated with allitridi became more shrunken and nepheloid, in which the microtubule networks disappeared, while the control cell exhibited an intact microtubule network. Contrasting with normal existence mainly in the cytoplasm, the cyclin B1 was expressed more significantly and concentrated in the nucleus after exposure to allitridi. Fluorescence intensity of cyclin B 1 protein in cells treated with allitridi was much more higher than that of control （P〈0.001）. Conclusion： Allitridican induce arrest of SGC-7901 cells in M phase, probably through enhancing microtubule depolymerization by elevating the expression of cyclin B1.展开更多
Transforming growth factor beta (TGF β) may cause cell cycle arrest, terminal differentiation, or apoptosis in most normal epithelial cells, whereas most malignant cell lines are resistant to TGF β. Mechanisms of...Transforming growth factor beta (TGF β) may cause cell cycle arrest, terminal differentiation, or apoptosis in most normal epithelial cells, whereas most malignant cell lines are resistant to TGF β. Mechanisms of resistance to TGF β caused by modulation of cell cycle regulators and/or inactivation of components of the TGF β signaling transduction pathway such as C myc and Smad4 are not well understood. To investigate the potential association between loss of sensitivity to TGF β and expression status of transforming growth factor receptor Ⅱ (TβRⅡ), Smad4, CDC25A and C myc in 14 cell lines derived from ovarian cancer, the expression levels of these genes were detected by semi quantitative RT PCR. Normal ovarian surface tissues were used as controls. The expression of TβRⅡ was detectable in all of 14 cell lines. The expression of Smad4 was decreased in 10 cell lines and 9 cell lines overexpressed CDC25A, as compared to normal controls. CDC25A gene was overexpressed with 88 % (8/9) in tumorigenic cell lines as determined by xenografts in nude mice, and only in 20 % (1/5) of non tumorigenic cell lines ( P <0.05). C myc was not overexpressed in any of these cell lines. The loss of sensitivity to TGF β of cell lines derived from ovarian cancers may be related to a decreased expression of Smad4, which mediates TGF β induced growth inhibition, and/or an overexpression of CDC25A. This overexpression of CDC25A correlates with increased tumorigenicity of ovarian cancer cell lines. The loss of sensitivity to TGF β is not associated with a lack of TβRⅡ.展开更多
文摘AIM： Esophageal squamous cell carcinoma is generally sensitive to chemoradiotherapy （CRT）, but some cases are not. Using a retrospective analysis, we aimed to identify the predictors of the response by esophageal squamous cell carcinoma to definitive CRT. METHODS： The intensities of expression of p53, Ki67, Bci-2, Bax, olclin D1, VEGF, CDC25B, and metallothionein （MT） were evaluated immunohistochemically in the biopsy specimens obtained before CRT, and the intensities of their expression were tested for correlations with the clinical effects of CRT. RESULTS： The esophageal squamous cell carcinomas with negative p53, positive CDC25B, and negative MT expression were found to be significantly more sensitive to CRT. In addition, p53 positivity and CDC25B positivity respomd well to CRT. CONCLUSION： Esophageal squamous cell carcinomas with negative p53,positive CDC25B, and negative MT expressions respond well to CRT. Even with p53 positivity, if with CDC25B positivity, CRT can be expected. 2005 The WJG Press and Elsevier Inc. All rights reserved
基金Supported by Heilongjiang Natural Science Foundation of China(C2017033)
文摘The aim of this experiment was to investigate whether FSH could regulate the proliferation of calf Sertoli cells and the relationship with CDC25 B through Wnt/β-catenin signaling pathway. The experimental method was to culture Sertoli cells with different concentrations of FSH(40, 80, 120 and 150 ng · mL) and to treat the cultured cells with XAV939(β-catenin inhibitor) and to detect the expression of CDC25 B, CDC2, C-MYC and β-catenin. The results of the experiment showed that FSH could promote the proliferation of cells and its effect was good at 80 ng · mLconcentration. FSH could promote the expression of CDC25 B, CDC2, C-MYC and β-catenin. The expression of C-MYC and β-catenin in group FSH+XAV939 was lower than that in group FSH. There was no difference in mRNA expression of CDC25 B in group FSH and group FSH+XAV939. The protein expression of CDC25 B in group FSH+XAV939 was lower than that in group FSH. The conclusion was that FSH could promote the proliferation of calf Sertoli cells through Wnt/β-catenin signaling pathway. CDC25 B was upregulated by FSH and CDC2 could promote the proliferation of calf Sertoli cells. The protein level of CDC25 B was affected by Wnt/β-catenin signaling pathway.
基金the National 10th Five-year Plan Key Technologies R & D Program of China(No.2004BA703B04-02)
文摘Objective： To learn the effect of allitridi on inducing mitotic arrest in human gastric cell line SGC-7901 and its possible mechanisms. Methods： We treated SGC-7901 cells with allitridi, and observed the proliferation inhibitory rate with MTT colometric assay, changes of cell cycle using flow cytometry and Switzerland-Giemsa＇s staining, and morphologic changes of the microtubule structure and location changes of cyclin BI expression using immunofluorescence and confocal laser scanning microscope. Furthermore, the expression of cyclin B1 was analyzed quantitatively using Leica confocal software. Results： SGC-7901 cells were inhibited after exposure to allitridi and the IC50 was 7.2μg/ml for 24 h, 20μg/ml for 72 h. When the cells were treated with allitridi at concentrations of 3, 6, and 9μg/ml for 24 h respectively, there was a declining tendency in the percentage of G0/G1 cell but an increasing tendency in GE/M cell in the allitridi treated group compared with that of control （P〈0.01）. When cells were treated allitridi at concentration of 6 μg/ml for 24 h, its mitotic index was much higher （P〈0.01） than that of control, suggesting that allitridi caused arrest of gastric cancer cells in M phase. The cells were treated with allitridi became more shrunken and nepheloid, in which the microtubule networks disappeared, while the control cell exhibited an intact microtubule network. Contrasting with normal existence mainly in the cytoplasm, the cyclin B1 was expressed more significantly and concentrated in the nucleus after exposure to allitridi. Fluorescence intensity of cyclin B 1 protein in cells treated with allitridi was much more higher than that of control （P〈0.001）. Conclusion： Allitridican induce arrest of SGC-7901 cells in M phase, probably through enhancing microtubule depolymerization by elevating the expression of cyclin B1.
文摘Transforming growth factor beta (TGF β) may cause cell cycle arrest, terminal differentiation, or apoptosis in most normal epithelial cells, whereas most malignant cell lines are resistant to TGF β. Mechanisms of resistance to TGF β caused by modulation of cell cycle regulators and/or inactivation of components of the TGF β signaling transduction pathway such as C myc and Smad4 are not well understood. To investigate the potential association between loss of sensitivity to TGF β and expression status of transforming growth factor receptor Ⅱ (TβRⅡ), Smad4, CDC25A and C myc in 14 cell lines derived from ovarian cancer, the expression levels of these genes were detected by semi quantitative RT PCR. Normal ovarian surface tissues were used as controls. The expression of TβRⅡ was detectable in all of 14 cell lines. The expression of Smad4 was decreased in 10 cell lines and 9 cell lines overexpressed CDC25A, as compared to normal controls. CDC25A gene was overexpressed with 88 % (8/9) in tumorigenic cell lines as determined by xenografts in nude mice, and only in 20 % (1/5) of non tumorigenic cell lines ( P <0.05). C myc was not overexpressed in any of these cell lines. The loss of sensitivity to TGF β of cell lines derived from ovarian cancers may be related to a decreased expression of Smad4, which mediates TGF β induced growth inhibition, and/or an overexpression of CDC25A. This overexpression of CDC25A correlates with increased tumorigenicity of ovarian cancer cell lines. The loss of sensitivity to TGF β is not associated with a lack of TβRⅡ.
