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学科主题口腔医学
Moesin regulates the motility of oral cancer cells via MT1-MMP and E-cadherin/p120-catenin adhesion complex
Li, Yao-yin; Zhou, Chuan-Xiang; Gao, Yan
关键词Moesin E-cadherin/p120-catenin Mt1-mmp Oral Squamous Cell Carcinoma Cell Motility
刊名ORAL ONCOLOGY
2015-10-01
DOI10.1016/j.oraloncology.2015.07.003
51期:10页:935-943
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology ; Dentistry, Oral Surgery & Medicine
研究领域[WOS]Oncology ; Dentistry, Oral Surgery & Medicine
关键词[WOS]E-CADHERIN ; MATRIX METALLOPROTEINASES ; TUMOR INVASION ; BREAST-CANCER ; ERM PROTEINS ; EZRIN ; METASTASIS ; CARCINOMA ; FAMILY ; PROGRESSION
英文摘要

Objective: The present study aimed to clarify the role of Moesin in oral squamous cell carcinoma (OSCC) progression, especially in regulation of cell motility.

Materials and Methods: Immunohistochemistry and western blotting were used to investigate the expression of Moesin, E-cadherin, p120-catenin and MT1-MMP in normal epithelia, dysplasia and OSCCs. Then, Moesin was knockdown by siRNA in OSCC cell lines, WSU-HN6 and CAL27, and the biological role of Moesin in cell adhesion and motility was evaluated by transwell system, cell spreading and aggregation assays. The interactions between Moesin, MT1-MMP and E-cadherin/p120-catenin complex were determined by co-immunoprecipitation and immunofluorescence.

Results: Moesin expression was found decreased in the membrane and increased in cytoplasm during the malignant transformation of oral epithelia, and cytoplasmic overexpression of Moesin correlated with nodal metastasis and poor prognosis of OSCCs. Furthermore, Moesin-silencing induced an increased cell-cell adhesion but decreased invasiveness, which was subsequently demonstrated might due to Moesin-mediated E-cadherin and p120-catenin interaction. Meantime, Moesin-silencing significantly down-regulated MT1-MMP expression, accompanied by reduced cell motility and impaired filopodia formation, which was also observed when MT1-MMP knockdown by RNAi or tissue inhibitor (TIMP2), indicating the involvement of MT1-MMP in Moesin-mediated cell motility. Finally, the relationship between Moesin, E-cadherin and MT1-MMP was confirmed in OSCC tissue samples.

Conclusion: Taken together, our results indicate Moesin may regulate cell motility through its interactions with MT1-MMP and E-cadherin/p120-catenin adhesion complex and cytoplasmic expression of Moesin correlates with nodal metastasis and poor prognosis of OSCCs, indicating Moesin may be a potential candidate for targeted gene therapy for OSCCs. (c) 2015 Elsevier Ltd. All rights reserved.

语种英语
WOS记录号WOS:000361240200010
引用统计
被引频次:3[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/52578
专题北京大学口腔医学院_口腔病理科
作者单位Peking Univ, Sch & Hosp Stomatol, Dept Oral Pathol, Beijing 100081, Peoples R China
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GB/T 7714
Li, Yao-yin,Zhou, Chuan-Xiang,Gao, Yan. Moesin regulates the motility of oral cancer cells via MT1-MMP and E-cadherin/p120-catenin adhesion complex[J]. ORAL ONCOLOGY,2015,51(10):935-943.
APA Li, Yao-yin,Zhou, Chuan-Xiang,&Gao, Yan.(2015).Moesin regulates the motility of oral cancer cells via MT1-MMP and E-cadherin/p120-catenin adhesion complex.ORAL ONCOLOGY,51(10),935-943.
MLA Li, Yao-yin,et al."Moesin regulates the motility of oral cancer cells via MT1-MMP and E-cadherin/p120-catenin adhesion complex".ORAL ONCOLOGY 51.10(2015):935-943.
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