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目的研究basigin(BSG,CD147)剪接异构体3(BSG3)在食管癌组织中的表达水平,及其对食管癌细胞功能的影响。方法免疫组织化学染色检测食管癌组织及正常食管组织BSG3的表达;实时定量PCR分析BSG1、BSG3在食管癌组织及正常食管组织中转录水平的差异;通过真核表达载体转染的方法在Eca109食管癌细胞中过表达BSG3,MTT法检测Eca109食管癌细胞的增殖活性,TranswellTM侵袭小室实验检测Eca109细胞的侵袭能力,划痕实验检测Eca109细胞的迁移能力。结果与正常食管组织相比,食管癌组织中BSG1和BSG3均高表达,过表达BSG3能够有效抑制Eca109细胞的增殖、侵袭和迁移能力。结论 BSG3在食管癌组织高表达,且能够拮抗BSG1的功能,抑制食管癌细胞增殖、侵袭和迁移能力。
Objective To study the expression of basalin (BSG, CD147) splicing isoform 3 (BSG3) in esophageal carcinoma and its effect on the function of esophageal carcinoma cells. Methods Immunohistochemical staining was used to detect the expression of BSG3 in esophageal cancer tissues and normal esophageal tissues. Real-time quantitative PCR was used to analyze the difference of transcript levels of BSG1 and BSG3 in esophageal cancer tissues and normal esophageal tissues. The eukaryotic expression vector was transfected into the esophagus The overexpression of BSG3 in cancer cells, the proliferation activity of Eca109 esophageal cancer cells by MTT assay, the invasion ability of Eca109 cells by TranswellTM invasion chamber assay, and the migration ability of Eca109 cells by scratch assay. Results Compared with normal esophageal tissues, both BSG1 and BSG3 were highly expressed in esophageal cancer tissues. Overexpression of BSG3 could effectively inhibit the proliferation, invasion and migration of Eca109 cells. Conclusion BSG3 is overexpressed in esophageal cancer tissues and can antagonize the function of BSG1 and inhibit the proliferation, invasion and migration of esophageal cancer cells.