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
目的:血管生成是肿瘤生长和转移的关键介质,CDC25B在包括三阴性乳腺癌(Triple-Negative Breast Cancer,TNBC)等恶性肿瘤作为肿瘤癌基因,但其对血管生成的生物学作用知之甚少,本研究旨在探讨CDC25B在TNBC血管生成中的确切功能和作用机制...目的:血管生成是肿瘤生长和转移的关键介质,CDC25B在包括三阴性乳腺癌(Triple-Negative Breast Cancer,TNBC)等恶性肿瘤作为肿瘤癌基因,但其对血管生成的生物学作用知之甚少,本研究旨在探讨CDC25B在TNBC血管生成中的确切功能和作用机制。方法:生信数据库分析CDC25B及其上游调控分子miR-141-3p在TNBC肿瘤组织中的表达,采用qRT-PCR分析CDC25B和miR-141-3p在TNBC细胞系中的表达。利用CCK-8和血管形成实验分析HUVEC细胞的增殖和血管形成能力,并通过Western blot检测VEGFA、VEGFR-2和VEGFR-3蛋白的表达。双荧光素酶报告实验被用于探索CDC25B和miR-141-3p之间的特异性相互作用。结果:本研究发现CDC25B在TNBC中表达上调,其高表达可以激活VEGF信号通路,沉默CDC25B后显著抑制了HUVEC细胞的增殖和血管生成,并降低了VEGFA、VEGFR-2和VEGFR-3蛋白的表达。此外,miR-141-3p在TNBC中表达下调,可以靶向抑制CDC25B的表达。过表达CDC25B可以逆转miR-141-3p过表达对HUVEC细胞增殖和血管生成的抑制作用。结论:miR-141-3p靶向CDC25B抑制VEGF通路抑制TNBC血管生成,为miR-141-3p/CDC25B/VEGF通路可能作为TNBC抗血管生成治疗的新选择提供理论依据。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
文摘目的:血管生成是肿瘤生长和转移的关键介质,CDC25B在包括三阴性乳腺癌(Triple-Negative Breast Cancer,TNBC)等恶性肿瘤作为肿瘤癌基因,但其对血管生成的生物学作用知之甚少,本研究旨在探讨CDC25B在TNBC血管生成中的确切功能和作用机制。方法:生信数据库分析CDC25B及其上游调控分子miR-141-3p在TNBC肿瘤组织中的表达,采用qRT-PCR分析CDC25B和miR-141-3p在TNBC细胞系中的表达。利用CCK-8和血管形成实验分析HUVEC细胞的增殖和血管形成能力,并通过Western blot检测VEGFA、VEGFR-2和VEGFR-3蛋白的表达。双荧光素酶报告实验被用于探索CDC25B和miR-141-3p之间的特异性相互作用。结果:本研究发现CDC25B在TNBC中表达上调,其高表达可以激活VEGF信号通路,沉默CDC25B后显著抑制了HUVEC细胞的增殖和血管生成,并降低了VEGFA、VEGFR-2和VEGFR-3蛋白的表达。此外,miR-141-3p在TNBC中表达下调,可以靶向抑制CDC25B的表达。过表达CDC25B可以逆转miR-141-3p过表达对HUVEC细胞增殖和血管生成的抑制作用。结论:miR-141-3p靶向CDC25B抑制VEGF通路抑制TNBC血管生成,为miR-141-3p/CDC25B/VEGF通路可能作为TNBC抗血管生成治疗的新选择提供理论依据。
