机构：[1]Department of Pathology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Province Guangdong, P.R. China中山大学附属第一医院[2]Department of Pathology, ShenZhen People’s Hospital, Second Clinical Medical College of Jinan University, Shenzhen, Guangdong, P.R. China深圳市康宁医院深圳市人民医院深圳医学信息中心[3]Department of Gynecology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Province Guangdong, P.R. China中山大学附属第一医院[4]Department of Stomatology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Province Guangdong, P.R. China中山大学附属第一医院[5]Department of Preventive Medicine and Biostatistics, School of Basic Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, P.R. China[6]Biomedical Engineering, University of Texas at El Paso, El Paso, Texas, USA[7]Department of Molecular and Medical Pharmacology, Crump Institute for Molecular Imaging (CIMI), California NanoSystems Institute (CNSI), University of California, Los Angeles, California, USA
Collagen triple helix repeat-containing 1 (CTHRC1) is aberrantly overexpressed in multiple malignant tumors. However, the expression characteristics and function of CTHRC1 in epithelial ovarian cancer (EOC) remain unclear. We found that CTHRC1 expression was up-regulated in the paraffin-embedded EOC tissues compared to borderline or benign tumor tissues. CTHRC1 expression was positively correlated with tumor size (p = 0.008), menopause (p = 0.037), clinical stage (p = 0.002) and lymph node metastasis (p < 0.001) and was also an important prognostic factor for the overall survival of EOC patients, as revealed by Kaplan-Meier analysis. CTHRC1 increased the invasive capabilities of EOC cells in vitro by activating the Wnt/beta-catenin signaling pathway. We showed that ectopic transfection of CTHRC1 in EOC cells up-regulated the expression of EMT markers such as N-cadherin and vimentin, and EMT-associated transcriptional factor Snail. Knockdown of CTHRC1 expression in EOC cells resulted in down-regulation of N-cadherin, vimentin, Snail and translocation of beta-catenin. Collectively, CTHRC1 may promote EOC metastasis through the induction of EMT process and serve as a potential biomarker for prognosis as well as a target for therapy.
基金：
National Natural Science Foundation of China (No. 30900650/H1615, 81372501/H1615, 81572260/H1615, 81172232/H1615 and 81172564/H1625), the Guangdong Natural Science Foundation (No. 2011B031800025, S2012010008378, S2012010008270, S2013010015327, 2013B021800126, 9451008901002146, 2015A020214010 and 2013B021800259) and the fundamental research funds for the central universities (2015ykzd07 and 11ykpy20).
第一作者机构：[1]Department of Pathology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Province Guangdong, P.R. China[3]Department of Gynecology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Province Guangdong, P.R. China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Hou Minzhi,Cheng Zhiqiang,Shen Hongwei,et al.High expression of CTHRC1 promotes EMT of epithelial ovarian cancer (EOC) and is associated with poor prognosis[J].ONCOTARGET.2015,6(34):35813-35829.doi:10.18632/oncotarget.5358.
APA：
Hou, Minzhi,Cheng, Zhiqiang,Shen, Hongwei,He, Shanyang,Li, Yang...&Ke, Zunfu.(2015).High expression of CTHRC1 promotes EMT of epithelial ovarian cancer (EOC) and is associated with poor prognosis.ONCOTARGET,6,(34)
MLA：
Hou, Minzhi,et al."High expression of CTHRC1 promotes EMT of epithelial ovarian cancer (EOC) and is associated with poor prognosis".ONCOTARGET 6..34(2015):35813-35829
