摘要
目的探讨大肠癌组织中E-钙粘素(E-cadherin)和基质金属蛋白酶-2(MMP-2)的表达及意义。方法应用免疫组织化学技术检测92例大肠癌及20例正常大肠组织中E-cadherin和MMP-2的表达,同时结合患者的临床病理资料进行分析。结果 E-cadherin在正常大肠组织中的阳性表达率为85%(17/20),高于大肠癌组织中52.2%(48/92)的表达率,两者具有显著差异性(p<0.01)。MMP-2在大肠癌组织中的表达率为71.7%(70/92),显著高于正常肠组织中35%(7/20)的表达率(p<0.01)。E-cadherin和MMP-2的表达都与大肠癌患者性别、年龄无明显相关,但与肿瘤浸润深度、临床分期、淋巴结转移密切相关(P<0.05);两者的表达具有负相关(r=-0.316,P<0.05)。结论 E-cadherin和MMP-2与大肠癌的发生发展密切相关。E-cadhein的正常表达将显著降低大肠癌的浸润和转移能力。而MMP-2蛋白阳性表达则促进大肠癌浸润和转移。E-cadherin和MMP-2的检测可以成为临床判断大肠癌的生物学行为的重要参考指标。
Objective To investigate the expression and clinical significance of E-cadherin and matrix metalloproteinase-2 (MMP-2) in color- ectal cancer. Methods The expression of E-cadherin and MMP-2 was detected in the tissues from 92 patients with colorectal cancer and 20 normal colorectal tissues by immunohistochemical assay. Results The positive expression rate of E-cadherin in normal tissues were 85% ( 17/ 20) ,higher than that in the colorectal cancer tissues 52.2% (48/92) ,there was a significance between them( p 〈0.01 ). While,the positive expression rate of MMP-2 in the colorectal cancer tissues was 71.7% (70/92) ,significantly higher than that in the normal tissues 35% (7/ 20) ( p 〈0. 01 ). The positive expression of E-cadhefin and MMP-2 both were associated with tumor depth,Dukes' stage,lymph node metas- tasis and distant metastasis, but not correlated with the gender, age. There is a negative relationship between the expression of E-cadherin and MMP-2 ( r = - 0. 316, P 〈 0.05 ). Conclusion The expression of E-cadherin, MMP-2 are both tightly correlated the genesis, development of colorectal cancer. Normal expression of the E-cadherin will lead to reduce the ability of invasion and metastasis in colorectal cancer. Meanwih- le, the positive expression of MMP-2 will promote the invasion and metastasis. Detecting the expression of E-cadherin, MMP-9 may be used an important prognostic indicator of invasion, metastasis, prognosis of colorectal cancer.
出处
《世界科技研究与发展》
CSCD
2013年第4期514-517,共4页
World Sci-Tech R&D
基金
重庆医科大学附属永川医院院内课题(YSQN2011037)资助