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目的探讨激活蛋白-1(AP-1)在结直肠癌及癌周组织中与DNA探针结合活性的变化及AP-1信号转导通路活化与结直肠癌转移的关系。方法采用电泳迁移率分析方法,检测30例结直肠癌手术切除标本及癌旁2cm、5cm组织和远癌切端组织中AP-1与DNA探针的结合活性;采用定量逆转录聚合酶链式反应方法检测各位点血管内皮细胞生长因子(VEGF)、基质金属蛋白酶-9(MMP-9)mRNA转录水平。结果结直肠癌组织AP-1与DNA探针的结合活性明显高于癌旁5cm组织和远癌切端组织(P<0.01);结直肠癌组织AP-1结合活性与肿瘤浸润程度、淋巴结转移呈明显正相关(P<0.01),而与肿瘤组织学分型以及肿瘤分化程度无显著相关性(P>0.05)。结直肠癌组织VEGF、MMP-9mRNA转录水平明显高于癌旁组织和癌远切端组织(P<0.01,P<0.05)。结直肠癌组织AP-1结合活性增强与VEGF、MMP-9高表达显著相关(P<0.01)。结论AP-1信号转导通路与结直肠癌浸润和转移过程密切相关;此通路的活化参与肿瘤转移过程中肿瘤新生血管生成和细胞外基质降解。
Objective To investigate the changes of the binding activity of AP-1 with DNA probes and the relationship between the activation of AP-1 signaling pathway and the metastasis of colorectal cancer in colorectal cancer and peri-cancerous tissues. Methods The electrophoretic mobility shift assay was used to detect the binding activity of AP-1 to DNA probe in 30 resected specimens of colorectal cancer and 2 cm, 5 cm tissues and distal cancer tissues. The expression of AP-1 was detected by quantitative reverse transcription-polymerase chain reaction Methods The levels of vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP-9) mRNA were detected at each site. Results The binding activity of AP-1 to DNA probe in colorectal cancer tissues was significantly higher than that in 5 cm adjacent tissues and distal incision tissues (P <0.01). The activity of AP-1 in colorectal cancer tissues was correlated with the degree of tumor invasion and lymph node metastasis (P <0.01), but not with tumor histological type and tumor differentiation (P> 0.05). The mRNA and protein expressions of VEGF and MMP-9 in colorectal cancer tissues were significantly higher than those in paracancerous tissues and distant tissues (P <0.01, P <0.05). Colorectal cancer tissue AP-1 binding activity and VEGF, MMP-9 expression was significantly correlated (P <0.01). Conclusion AP-1 signal transduction pathway is closely related to the invasion and metastasis of colorectal cancer. The activation of this pathway is involved in tumor angiogenesis and extracellular matrix degradation during tumor metastasis.