Differential expression of Kindlin-1 and Kindlin-2 correlates with esophageal cancer progression and epidemiology

被引:0
|
作者
Peng Wang [1 ,2 ]
Jun Zhan [1 ]
Jiagui Song [1 ]
Yunling Wang [3 ]
Weigang Fang [1 ,2 ]
Zhihua Liu [4 ]
Hongquan Zhang [1 ]
机构
[1] Department of Anatomy,Histology and Embryology,Key Laboratory of Carcinogenesis and Translational Research,Ministry of Education,and State Key Laboratory of Natural and Biominelic Drugs,Peking University Health Science Center
[2] Department of Pathology,Peking University Health Science Center
[3] Institute of Cardiovascular Research,Peking University Health Science Center
[4] State Key Laboratory of Motecular Oncology,National Cancer Center/Cancer Hospital,Chinese Academy of Medical Sciences and Peking Union Medical College
基金
北京市自然科学基金; 中国国家自然科学基金;
关键词
Kindlin-1; Kindlin-2; esophageal cancer; epidemiology;
D O I
暂无
中图分类号
R735.1 [食管肿瘤];
学科分类号
100214 ;
摘要
Esophageal cancer(EC) is one of the most lethal malignancies in China, but the etiology and risk factors remain unclear.The integrin-interacting proteins Kindlin-1 and Kindlin-2 are focal adhesion molecules that activate transmembrane receptor integrins and regulate tumor cell growth, invasion, and metastasis. Here, we report that Kindlin-I and Kindlin-2 are differentially expressed among Chinese EC patients. For this, Kindlin-1 and Kindlin-2 expression was evaluated in 220 EC patients by immunohistochemistry(IHC) and found to be correlated with the EC progression, along with a variety of epidemiologic parameters,including smoking,family EC history,and EC invasion status. Moreover,data downloaded from the Oncomine database revealed that both Kindlin-1 and Kindlin-2 were upregulated in ECs compared with normal esophageal tissues; although Kindlin-1 was highly expressed in well-differentiated tumors, whereas Kindlin-2 was more prevalent in poorly differentiated tumors. Collectively, these data suggest that Kindlin-1 may inhibit, while Kindlin-2 may promote, EC progression. This study,for the first time, linked the expression of Kindlin-1 and Kindlin-2 with EC family genetic background and living habits, which may help further our understanding of the various causes of EC.
引用
收藏
页码:1214 / 1222
页数:9
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