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
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.
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.
