Literature DB >> 26221280

Snail promotes epithelial-mesenchymal transition and invasiveness in human ovarian cancer cells.

Yu-Lou Wang1, Xue-Min Zhao1, Zhi-Feng Shuai2, Chun-Yan Li2, Qing-Yang Bai2, Xiu-Wen Yu2, Qiu-Ting Wen2.   

Abstract

There are limited reports with respect to the study on the epithelium-mesenchymal transformation (EMT) mediated by Snail in the ovarian cancer. This study detected the expression of Snail and related EMT markers in the ovarian cancer tissues, and explored the possible molecular mechanism of EMT mediated by Snail in the metastasis of ovarian cancer. The patients diagnosed with ovarian cancer according to the pathology were recruited in this study during 2010-2014. The carcinoma tissue and normal tissue adjacent to carcinoma were surgically obtained from patients. The genes of E-cadherin, β-catenin, Fibronectin and N-cadherin were detected using the RT-PCR. The 64 patients were recruited and diagnosed as ovarian cancer by pathological examination. The expression levels of Snail, Fibronectin and N-cadherin in the stage III and IV were higher than those in the stage I and II, respectively (all P < 0.05). However, the expression levels of E-cadherin and β-catenin decreased along with the stage developed (trend test, both P < 0.05), respectively. The expression of Snail was positively correlated with the expression of Fibronectin, N-cadherin, but negatively correlated with the expression of E-cadherin and β-catenin. The number of A2780 cells entering into the lower compartment in the group of carcinoma tissue were significantly higher than that in the group of normal tissue after transfected with Snail expression vector. While, the invasion ability of A2780 significantly reduced after RNAi-Snail. The correlation between Snail and invasion and metastasis of ovarian cancer and epithelial-mesenchymal transition based on tissue and cell levels, and to some extent explored the molecular mechanism of the EMT process mediated by Snail.

Entities:  

Keywords:  Snail; epithelium-mesenchymal transformation; molecular mechanism; ovarian cancer

Year:  2015        PMID: 26221280      PMCID: PMC4509225     

Source DB:  PubMed          Journal:  Int J Clin Exp Med        ISSN: 1940-5901


  20 in total

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