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作 者:曾志梅[1,2] 梁永辉[1] 杨嶷芳[1] 窦晓清[1] 陈贤明[1,2]
机构地区:[1]南京军区福州总医院耳鼻咽喉头颈外科,福建福州350025 [2]福建医科大学福州总临床医学院,福建福州350025
出 处:《中国耳鼻咽喉颅底外科杂志》2011年第2期95-99,共5页Chinese Journal of Otorhinolaryngology-skull Base Surgery
摘 要:目的探讨RECK与MMP-2蛋白表达与下咽癌侵润和转移的关系。方法应用手术方法取下咽癌原发灶、癌旁组织及淋巴节转移组织22例,另取良性病变(声带息肉)10例作为对照,应用免疫组化检测RECK、MMP-2蛋白表达,并与下咽癌不同临床分期进行相关性分析。结果 RECK的表达水平在下咽癌原发灶、转移灶中均明显低于癌旁组织及良性病变组织;下咽癌组织中有淋巴结转移组表达水平低于无淋巴结转移组,临床Ⅲ、Ⅳ期低于临床Ⅰ、Ⅱ期。MMP-2的表达水平在下咽癌原发灶、转移灶中均明显高于癌旁组织及良性病变组织;下咽癌组织中有淋巴结转移组的表达水平高于无淋巴结转移组,临床Ⅲ、Ⅳ期高于临床Ⅰ、Ⅱ期。两者的蛋白表达水平呈负相关,相关系数为-0.732。结论 RECK的表达水平与下咽癌的侵袭与转移有关,其调控机制可能与RECK蛋白能抑制MMP-2蛋白的表达有关。Objective To study the expression of reversion inducing cysteine rich protein with Kazal motifs(RECK) and matrix metalloprotease-2(MMP-2) in hypopharyngeal carcinoma,and to explore the relationship between them.Methods The expression of RECK and MMP-2 was detected in specimens(including tumor tissue,metastatic lymph node and adjacent normal tissue) from 22 cases with hypopharynx carcinoma and 10 specimens of benign lession(vocal polyp) with immumohistochemistry.The tumor tissue,metastatic lymph node and adjacent normal tissue were detected separately.Results The expression of RECK in primary loci and metastatic lymph node was significantly lower than that in adjacent normal tissue and the benign lession.The expression of RECK in the primary loci with lymphatic metastasis was lower than that without lymphatic metastasis.The expression of RECK in the primary loci of Ⅲ,Ⅳ stages was lower than those of the Ⅰ,Ⅱ stages.The expressions of MMP-2 in primary loci and metastatic lymph node was significantly higher than that in adjacent normal tissue and the benign lession.The expression of MMP-2 in the primary loci with lymphatic metastasis was higher than that without lymphatic metastasis.The expression of MMP-2 in the primary loci of Ⅲ,Ⅳ stages was higher than that of the Ⅰ,Ⅱ stages.The expression of RECK was negatively correlated with that of MMP-2(γ=-0.732).Conclusion The expression of RECK may be related to invasion and metastasis of hypopharynx carcinoma with the possible mechanism by inhibiting the expression of MMP-2.
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