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Review Article | Open Access

Epithelial protein lost in neoplasm (EPLIN): Beyond a tumor suppressor

Daqing Wua,b,( )
Georgia Cancer Center and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, GA, USA
MetCure Therapeutics LLC, Atlanta, GA, USA

Peer review under responsibility of Chongqing Medical University.

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Abstract

The majority of cancer-related deaths are caused by tumor recurrence, metastasis and therapeutic resistance. During the late stages of tumor progression, multiple factors are involved, including the downregulation and/or loss of function of metastasis suppressors. Epithelial protein lost in neoplasm (EPLIN), an actin-binding protein, was initially identified as a putative tumor suppressor that is frequently downregulated in epithelial tumors. Recent evidence indicates that EPLIN may negatively regulate epithelia-to-mesenchymal transition (EMT), a crucial process by which cancer cells acquire invasive capabilities and therapeutic resistance. Importantly, downregulation of EPLIN is associated with clinical metastasis in a variety of solid tumors, suggesting that EPLIN could be a suppressor of metastasis. In this review, I will discuss the regulation and function of EPLIN in human cancer cells and explore the clinical significance of EPLIN in metastatic disease.

Keywords

Tumor suppressorActin cytoskeletonChemoresistanceEpithelial-to-mesenchymal transitionEPLINMetastasis suppressor

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Genes & Diseases
Volume 4 Issue 2,
June 2017
Pages 100-107
DOI: 10.1016/j.gendis.2017.03.002
Cite this article:
Wu D. Epithelial protein lost in neoplasm (EPLIN): Beyond a tumor suppressor. Genes & Diseases, 2017, 4(2): 100-107. https://doi.org/10.1016/j.gendis.2017.03.002

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Received: 13 December 2016
Accepted: 25 March 2017
Published: 01 April 2017
© 2017, Chongqing Medical University.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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