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Metadherin regulates epithelial–mesenchymal transition in carcinoma

Authors Wang Z, Tang Z, Yin Z, Wei Y, Liu L, Yan B, Zhou K, Nian Y, Gao Y, Yang J

Received 19 January 2016

Accepted for publication 19 February 2016

Published 21 April 2016 Volume 2016:9 Pages 2429—2436


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Ram Prasad

Peer reviewer comments 3

Editor who approved publication: Dr William Cho

Zhao Wang,1,2 Zheng-yan Tang,2 Zhuo Yin,1 Yong-bao Wei,1,3 Long-fei Liu,2 Bin Yan,1 Ke-qin Zhou,1 Ye-qi Nian,1 Yun-liang Gao,1 Jin-rui Yang1

1Department of Urology, The Second Xiangya Hospital, Central South University, Fu Rong District, Changsha, 2Department of Urology, Xiangya Hospital, Central South University, Kai Fu District, 3Department of Urology, Fujian Provincial Hospital, The Teaching Hospital of Fujian Medical University, Fuzhou, People’s Republic of China

Abstract: Metadherin (MTDH) was first identified in primary human fetal astrocytes exposed to HIV-1 in 2002 and then recognized as an important oncogene mediating tumorigenesis, progression, invasiveness, and metastasis of carcinomas. Epithelial–mesenchymal transition (EMT) is a vital process in embryonic development, organ repair, and cancer progression. MTDH and EMT have also been proved to be related to the prognosis of patients with cancers. Recent studies reveal a relationship between MTDH overexpression and EMT in some malignancies. This review highlights the overexpression of MTDH and EMT in cancers and their correlations in clinical studies. Positive correlations have been established between MTDH and mesenchymal biomarkers, and negative correlations between MTDH and epithelial biomarkers have also been established. Furthermore, experiments reveal EMT regulated by MTDH, and some signal pathways have been established. Some anticancer drugs targeting MTDH and EMT are introduced in this review. Some perspectives concerning EMT regulation by MTDH are also presented in this review.

Keywords: signal pathway, chemoprevention, oncogene, biomarker, progression, therapeutic target

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