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

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	Differential expression of Kindlin-1 and Kindlin-2 correlates with esophageal cancer progression and epidemiology
其他题名	Differential expression of Kindlin-1 and Kindlin-2 correlates with esophageal cancer progression and epidemiology
	2017
发表期刊	SCIENCE CHINA-LIFE SCIENCES
ISSN	1674-7305
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-1 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.
其他摘要	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-1 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.
关键词	SQUAMOUS-CELL CARCINOMA HEPATOCELLULAR-CARCINOMA UP-REGULATION PROMOTES INVASION PROLIFERATION INVASIVENESS MIGRATION FAMILY LUNG Kindlin-1 Kindlin-2 esophageal cancer epidemiology
收录类别	CSCD
语种	英语
资助项目	[Ministry of Science and Technology of China] ; [National Natural Science Foundation of China] ; [Beijing Natural Science Foundation] ; [111 Project of the Ministry of Education] ; [Peking University] ; [Leading Academic Discipline Project of Beijing Education Bureau]
CSCD记录号	CSCD:6150316
引用统计	被引频次：1[CSCD] [CSCD记录]
文献类型	期刊论文
条目标识符	http://ir.hfcas.ac.cn:8080/handle/334002/69976
专题	中国科学院合肥物质科学研究院
推荐引用方式 GB/T 7714	. Differential expression of Kindlin-1 and Kindlin-2 correlates with esophageal cancer progression and epidemiology[J]. SCIENCE CHINA-LIFE SCIENCES,2017,60.
APA	(2017).Differential expression of Kindlin-1 and Kindlin-2 correlates with esophageal cancer progression and epidemiology.SCIENCE CHINA-LIFE SCIENCES,60.
MLA	"Differential expression of Kindlin-1 and Kindlin-2 correlates with esophageal cancer progression and epidemiology".SCIENCE CHINA-LIFE SCIENCES 60(2017).