MRGBP as a potential biomarker for the malignancy of pancreatic ductal adenocarcinoma
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Feng Ding1,2, Shuang Zhang3, Shaoyang Gao4, Jian Shang1,2, Yanxia Li5, Ning Cui5 and Qiu Zhao1,2
1Department of Gastroenterology/Hepatology, ZhongNan Hospital of Wuhan University, Wuhan 430071, China
2The Hubei Clinical Center & Key Laboratory of Intestinal & Colorectal Diseases, Wuhan 430071, China
3Laboratory of Clinical Immunology, Wuhan No.1 Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China
4Department of Pathology, Hubei Cancer Hospital, Wuhan 430079, China
5Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, China
Qiu Zhao, email: [email protected]
Keywords: MRGBP, pancreatic ductal adenocarcinoma, biomarker, upregulation
Received: February 24, 2017 Accepted: April 12, 2017 Published: July 22, 2017
MORF4-related gene-binding protein (MRGBP), which is also known as chromosome 20 open reading frame 20 (C20orf20), is commonly highly expressed in several types of malignant tumors and tumor progression. However, the expression pattern and underlying mechanism of MRGBP in pancreatic ductal adenocarcinoma (PDAC) remain unknown. In the study, we found that MRGBP was frequently upregulated in PDAC tissues and cell lines. In addition, the upregulation of MRGBP was positively associated with TNM stage, T classification, and poor prognosis. Knockdown of MRGBP in the PDAC cell lines ASPC-1 and Mia PaCa-2 by transiently transfected with small interfering RNA (siRNA) drastically attenuated the proliferation, migration, and invasion of those cells, whereas ectopic MRGBP overexpression in BxPC-3 cells produced exactly the opposite effect. Furthermore, we also found that overexpression of MRGBP remarkably led to cell morphological changes and induced an increased expression of mesenchymal marker Vimentin, whereas a decreased expression of epithelial marker E-cadherin. Taken together, this study indicates that MRGBP acts as a tumor oncogene in PDAC and is a promising target of carcinogenesis.
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