Aberrant expression of Notch1/numb/snail signaling, an epithelial mesenchymal transition related pathway, in adenomyosis

被引:39
作者
Qi, Shasha [1 ]
Zhao, Xingbo [1 ]
Li, Mingjiang [1 ]
Zhang, Xiaohui [1 ]
Lu, Zhenzhen [1 ]
Yang, Chunrun [1 ]
Zhang, Chunhua [1 ]
Zhang, Hui [1 ]
Zhang, Na [2 ]
机构
[1] Shandong Univ, Shandong Prov Hosp, Dept Obstet & Gynecol, Jinan 250021, Shandong, Peoples R China
[2] Shandong Univ, Shandong Prov Hosp, Dept Anesthesiol & Surg, Jinan 250021, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
Adenomyosis; Epithelial Mesenchymal Transition; Notch1/Numb/Snail Signaling; Slug; E-CADHERIN EXPRESSION; CELL-FATE; PROSTATE-CANCER; SNAIL; NUMB; TRANSCRIPTION; NOTCH1; EMT; MIGRATION; RECEPTOR;
D O I
10.1186/s12958-015-0084-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Epithelial mesenchymal transition (EMT) is involved in the pathogenesis of adenomyosis, and Notch signaling is crucial to EMT. The objective of this study was to explore Notch1/Numb/Snail signaling in adenomyosis. Methods: The expression levels of the members of the Notch1/Numb/Snail signaling cascade in normal endometria (proliferative phase: n = 15; secretory phase: n = 15; postmenopausal phase: n = 15) and adenomyotic endometria (proliferative phase: n = 15; secretory phase: n = 15) were determined by immunohistochemistry analysis. Results: We found that the expressions of Notch1 and the EMT-related proteins N-cadherin, Snail and Slug were upregulated in the ectopic endometrium of adenomyosis compared with normal endometrium. Numb, a negative regulator of Notch signaling, was significantly decreased in adenomyosis. In addition, reduced immunoexpression of E-cadherin was observed in adenomyosis. Conclusions: We conclude that Notch1/Numb/Snail signaling plays an important role in the pathogenesis and development of adenomyosis.
引用
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页数:10
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