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      Expression and Function of ZEB1 in the Cornea

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          Abstract

          ZEB1 is an important transcription factor for epithelial to mesenchymal transition (EMT) and in the regulation of cell differentiation and transformation. In the cornea, ZEB1 presents in all three layers: the epithelium, the stroma and the endothelium. Mutations of ZEB1 have been linked to multiple corneal genetic defects, particularly to the corneal dystrophies including keratoconus (KD), Fuchs endothelial corneal dystrophy (FECD), and posterior polymorphous corneal dystrophy (PPCD). Accumulating evidence indicates that dysfunction of ZEB1 may affect corneal stem cell homeostasis, and cause corneal cell apoptosis, stromal fibrosis, angiogenesis, squamous metaplasia. Understanding how ZEB1 regulates the initiation and progression of these disorders will help us in targeting ZEB1 for potential avenues to generate therapeutics to treat various ZEB1-related disorders.

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          Most cited references65

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          Molecular mechanisms of epithelial-mesenchymal transition.

          Samy Lamouille, Jian Xu, Rik Derynck (2014)
          The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound healing and stem cell behaviour, and contributes pathologically to fibrosis and cancer progression. This switch in cell differentiation and behaviour is mediated by key transcription factors, including SNAIL, zinc-finger E-box-binding (ZEB) and basic helix-loop-helix transcription factors, the functions of which are finely regulated at the transcriptional, translational and post-translational levels. The reprogramming of gene expression during EMT, as well as non-transcriptional changes, are initiated and controlled by signalling pathways that respond to extracellular cues. Among these, transforming growth factor-β (TGFβ) family signalling has a predominant role; however, the convergence of signalling pathways is essential for EMT.
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            ZEB1: at the crossroads of epithelial-mesenchymal transition, metastasis and therapy resistance.

            Peijing Zhang, Yutong Sun, Li Ma (2015)
            Zinc finger E-box binding homeobox 1 (ZEB1) is a transcription factor that promotes tumor invasion and metastasis by inducing epithelial-mesenchymal transition (EMT) in carcinoma cells. EMT not only plays an important role in embryonic development and malignant progression, but is also implicated in cancer therapy resistance. It has been hypothesized that carcinoma cells that have undergone EMT acquire cancer stem cell properties including self-renewal, chemoresistance and radioresistance. However, our recent data indicate that ZEB1 regulates radioresistance in breast cancer cells through an EMT-independent mechanism. In this Perspective, we review different mechanisms by which ZEB1 regulates tumor progression and treatment resistance. Based on studies by us and others, we propose that it is specific EMT inducers like ZEB1, but not the epithelial or mesenchymal state itself, that dictate cancer stem cell properties.
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              Molecular pathways: linking tumor microenvironment to epithelial-mesenchymal transition in metastasis.

              Hae-Yun Jung, Laurent Fattet, Jing Yang (2015)
              During tumor development, tumor cells constantly communicate with the surrounding microenvironment through both biochemical and biophysical cues. In particular, the tumor microenvironment can instruct carcinoma cells to undergo a morphogenesis program termed epithelial-to-mesenchymal transition (EMT) to facilitate local invasion and metastatic dissemination. Growing evidence uncovered a plethora of microenvironmental factors in promoting EMT, including proinflammatory cytokines secreted by locally activated stromal cells, hypoxia conditions, extracellular matrix components, and mechanical properties. Here, we review various biochemical and biophysical factors in the tumor microenvironment that directly impinge upon the EMT program. Specifically, cytokines such as TGFβ, TNFα, and IL6 and hypoxia are capable of inducing EMT in various tumors. Several extracellular matrix (ECM) proteins, including collagen-I, fibronectin, and hyaluronan, and ECM remodeling via extracellular lysyl oxidase are also implicated in regulating EMT. In preclinical studies and ongoing clinical trials, targeting these tumor microenvironmental signals has shown promises in halting tumor progression in various human cancers.
              Article 0 comments Cited 130 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Alexander V. Ljubimov: Role: Academic Editor
                Dimitrios Karamichos: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 16 April 2021
                Publication date Collection: April 2021
                Volume: 10
                Issue: 4
                Electronic Location Identifier: 925
                Affiliations
                [1 ]Department of Medicine, University of Louisville School of Medicine, Louisville, KY 40202, USA; yingnan.zhang@ 123456louisville.edu (Y.Z.); dcdean01@ 123456louisville.edu (D.C.D.)
                [2 ]James Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY 40202, USA
                [3 ]Department of Ophthalmology, The Second Xiangya Hospital of Central South China University, Changsha 410011, China; liuxiao-doctor@ 123456163.com
                [4 ]Department of Ophthalmology, The Third People’s Hospital of Dalian, Dalian Medical University, Dalian 116033, China; liangwei_6227327@ 123456126.com
                [5 ]Birth Defects Center, University of Louisville School of Dentistry, Louisville, KY 40202, USA
                Author notes
                [* ]Correspondence: lijunzhangw@ 123456gmail.com (L.Z.); y0liu016@ 123456louisville.edu (Y.L.); Tel.: +86-181-4117-8066 (L.Z.); +1-502-852-8669 (Y.L.)
                [†]

                Y.Z. and X.L. contribute equally.

                Author information
                https://orcid.org/0000-0003-1090-0865
                Article
                Publisher ID: cells-10-00925
                DOI: 10.3390/cells10040925
                PMC ID: 8074155
                PubMed ID: 33923743
                SO-VID: 141dc231-49fb-43c4-a824-ad62928d385a
                Copyright © © 2021 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 28 February 2021
                Date accepted : 14 April 2021
                Categories
                Subject: Review

                Keywords: zeb1,corneal dystrophies,stem cell homeostasis,wound healing,inflammation,neovascularization
                Data availability:
                Keywords: zeb1, corneal dystrophies, stem cell homeostasis, wound healing, inflammation, neovascularization

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