Abstract
Epithelial ovarian cancer (EOC) is the leading cause of death among gynecologic malignancies. Despite great efforts to improve early detection and optimize chemotherapeutic regimens, the 5-year survival rate is only 30% for patients presenting with late-stage ovarian cancer. The high mortality of this disease is due to late diagnosis in over 70% of ovarian cancer cases. A class of small noncoding RNAs, or microRNAs, was found to regulate gene expression at the post-transcriptional level. Some, but not all, of the data indicated that the miR-200 family was dysregulated in a variety of malignancies. In this study, we demonstrated that miR-200a and E-cadherin were significantly upregulated in EOC compared to benign epithelial ovarian cysts and normal ovarian tissues. However, further stratification of the subject indicated that the expression levels of miR-200a were significantly downregulated in late-stage (FIGO III+V) and grade 3 groups compared with early stage (FIGO I+II) and grade 1 to 2 groups. Similarly, relatively low levels of miR-200a were observed in the lymph compared to the node-negative group. E-cadherin expression was found to be absent in normal ovarian tissue and was frequently expressed in benign epithelial ovarian cysts, with absence or low levels observed in late-stage ovarian cancers. There was a significantly positive correlation between miR-200a and E-cadherin in EOC. The biphasic expression pattern suggested that miR-200a levels may serve as novel biomarkers for the early detection of EOC, and miR-200a and E-cadherin are candidate targets for the development of new treatment modalities against ovarian cancer.
Keywords: Epithelial ovarian cancer, microRNA, miR-200a, E-cadherin.
Current Pharmaceutical Design
Title:The Biphasic Expression Pattern of miR-200a and E-cadherin in Epithelial Ovarian Cancer and its Correlation with Clinicopathological Features
Volume: 20 Issue: 11
Author(s): Shaohua Xu, Peizhen Xu, Wei Wu, Yangjun Ou, Juan Xu, Guanghua Zhang, Jinping Li and Guofeng Xu
Affiliation:
Keywords: Epithelial ovarian cancer, microRNA, miR-200a, E-cadherin.
Abstract: Epithelial ovarian cancer (EOC) is the leading cause of death among gynecologic malignancies. Despite great efforts to improve early detection and optimize chemotherapeutic regimens, the 5-year survival rate is only 30% for patients presenting with late-stage ovarian cancer. The high mortality of this disease is due to late diagnosis in over 70% of ovarian cancer cases. A class of small noncoding RNAs, or microRNAs, was found to regulate gene expression at the post-transcriptional level. Some, but not all, of the data indicated that the miR-200 family was dysregulated in a variety of malignancies. In this study, we demonstrated that miR-200a and E-cadherin were significantly upregulated in EOC compared to benign epithelial ovarian cysts and normal ovarian tissues. However, further stratification of the subject indicated that the expression levels of miR-200a were significantly downregulated in late-stage (FIGO III+V) and grade 3 groups compared with early stage (FIGO I+II) and grade 1 to 2 groups. Similarly, relatively low levels of miR-200a were observed in the lymph compared to the node-negative group. E-cadherin expression was found to be absent in normal ovarian tissue and was frequently expressed in benign epithelial ovarian cysts, with absence or low levels observed in late-stage ovarian cancers. There was a significantly positive correlation between miR-200a and E-cadherin in EOC. The biphasic expression pattern suggested that miR-200a levels may serve as novel biomarkers for the early detection of EOC, and miR-200a and E-cadherin are candidate targets for the development of new treatment modalities against ovarian cancer.
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Cite this article as:
Xu Shaohua, Xu Peizhen, Wu Wei, Ou Yangjun, Xu Juan, Zhang Guanghua, Li Jinping and Xu Guofeng, The Biphasic Expression Pattern of miR-200a and E-cadherin in Epithelial Ovarian Cancer and its Correlation with Clinicopathological Features, Current Pharmaceutical Design 2014; 20 (11) . https://dx.doi.org/10.2174/13816128113199990523
DOI https://dx.doi.org/10.2174/13816128113199990523 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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