Document Detail


Roles of ezrin in the growth and invasiveness of esophageal squamous carcinoma cells.
MedLine Citation:
PMID:  19165868     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ezrin, which crosslinks the cytoskeleton and plasma membrane, is involved in the growth and metastatic potential of cancer cells. Ezrin expression in esophageal squamous cell carcinoma (ESCC) was described recently, but its roles and the underlying mechanism(s) remain unclear. In our study, we first showed that ezrin in ESCC cell is expressed in the nucleus as well as in the cytoplasm and plasma membrane. Then, by using RNAi, we revealed that interference of ezrin expression suppressed the growth, adhesion and invasiveness of ESCC cells. Tumorigenesis experiments revealed that ezrin may directly regulate tumor formation in vivo. To explore the molecular mechanisms through which ezrin contributes to the proliferation and invasiveness of ESCC cells, we used cDNA microarrays to analyze ezrin knockdown cells and the control cells; of 39,000 genes examined, 297 were differentially expressed upon ezrin knockdown, including some proliferation- and invasiveness-related genes such as ATF3, CTGF and CYR61. Furthermore, pathway analysis showed that ezrin knockdown led to decreased activation of the TGF-beta and MAPK pathways, and ezrin-mediated cell invasiveness alteration was dependent on the activation of these pathways. Finally, immunohistochemical staining on 80 ESCC specimens and 50 normal esophageal mucosae revealed that the expression levels of 3 altered genes involved in the regulation of cell proliferation and tumor metastasis, including CTGF, CYR61 and ATF3, were altered in ESCCs, and their expression pattern correlated with ezrin expression. Taken together, we propose that ezrin might function in the growth and invasiveness of ESCC cells through the MAPK and TGF-beta pathways.
Authors:
Jian-Jun Xie; Li-Yan Xu; Yang-Min Xie; Hai-Hua Zhang; Wei-Jia Cai; Fei Zhou; Zhong-Ying Shen; En-Min Li
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of cancer. Journal international du cancer     Volume:  124     ISSN:  1097-0215     ISO Abbreviation:  Int. J. Cancer     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-04-01     Completed Date:  2009-04-14     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0042124     Medline TA:  Int J Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2549-58     Citation Subset:  IM    
Affiliation:
Department of Biochemistry and Molecular Biology, Medical College of Shantou University, Shantou, People's Republic of China.
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MeSH Terms
Descriptor/Qualifier:
Activating Transcription Factor 3 / genetics
Animals
Carcinoma, Squamous Cell / pathology
Cell Adhesion
Cell Line, Tumor
Cell Movement
Cell Proliferation
Connective Tissue Growth Factor / genetics
Cysteine-Rich Protein 61 / genetics
Cytoskeletal Proteins / antagonists & inhibitors,  genetics,  physiology*
Esophageal Neoplasms / pathology
Extracellular Signal-Regulated MAP Kinases / physiology
Humans
Mice
Neoplasm Invasiveness
RNA, Small Interfering / genetics
Transforming Growth Factor beta1 / physiology
Chemical
Reg. No./Substance:
0/ATF3 protein, human; 0/Activating Transcription Factor 3; 0/CTGF protein, human; 0/CYR61 protein, human; 0/Cysteine-Rich Protein 61; 0/Cytoskeletal Proteins; 0/RNA, Small Interfering; 0/Transforming Growth Factor beta1; 0/ezrin; 139568-91-5/Connective Tissue Growth Factor; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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