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EGF Receptor (EGFR) Trafficking Pathways: From Epithelial Cell Functions to Epithelial Carcinomas

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A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 9644

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Special Issue Editor

Prof. Cathleen R. Carlin

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Guest Editor

Department of Molecular Biology and Microbiology, Case Comprehensive Cancer Center, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA
Interests: receptor tyrosine kinases; intracellular trafficking; epithelial cell polarity; cholesterol homeostasis; viral pathogenesis;

Special Issue Information

Dear Colleagues,

I hope this message finds you and those you hold dear safe and in good health during these challenging times.

I am reaching out to let you know that we are organizing a Special Issue on ‘EGF Receptor Trafficking Pathways: From Epithelial Cell Functions to Epithelial Carcinomas’ that we think you may be interested in contributing to.

Your expertise in the field will be a valuable contribution to this Special Issue. Apart from potential research articles that you might consider to submit, I encourage you and your co-workers to prepare a review on any basic or applied topic which could contribute to the advancement and understanding of physiological EGF receptor biology in polarized epithelial cells, its misappropriation in epithelial carcinomas, and the current state of therapeutic strategies for overcoming resistance to EGF receptor-targeted drugs.

We are looking forward to your positive reply to this call!

Stay safe and healthy.

Prof. Cathleen R. Carlin
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

EGF receptor
Epithelial cell polarity
Epithelial carcinoma
Therapeutic resistance

Published Papers (2 papers)

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Research

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16 pages, 4245 KiB

Open AccessArticle

Lactobacillus casei and Epidermal Growth Factor Prevent Osmotic Stress-Induced Tight Junction Disruption in Caco-2 Cell Monolayers

by Geetha Samak, Rupa Rao and Radhakrishna Rao

Cells 2021, 10(12), 3578; https://doi.org/10.3390/cells10123578 - 18 Dec 2021

Cited by 6 | Viewed by 2893

Abstract

Osmotic stress plays a crucial role in the pathogenesis of many gastrointestinal diseases. Lactobacillus casei and epidermal growth factor (EGF) effects on the osmotic stress-induced epithelial junctional disruption and barrier dysfunction were investigated. Caco-2 cell monolayers were exposed to osmotic stress in the presence or absence of L. casei or EGF, and the barrier function was evaluated by measuring inulin permeability. Tight junction (TJ) and adherens junction integrity were assessed by immunofluorescence confocal microscopy. The role of signaling molecules in the L. casei and EGF effects was determined by using selective inhibitors. Data show that pretreatment of cell monolayers with L. casei or EGF attenuates osmotic stress-induced TJ and adherens junction disruption and barrier dysfunction. EGF also blocked osmotic stress-induced actin cytoskeleton remodeling. U0126 (MEK1/2 inhibitor), the MAP kinase inhibitor, blocked EGF-mediated epithelial protection from osmotic stress. In contrast, the L. casei-mediated epithelial protection from osmotic stress was unaffected by U0126, AG1478 (EGFR tyrosine kinase inhibitor), SP600125 (JNK1/2 inhibitor), or SB202190 (P38 MAP kinase inhibitor). On the other hand, Ro-32-0432 (PKC inhibitor) blocked the L. casei-mediated prevention of osmotic stress-induced TJ disruption and barrier dysfunction. The combination of EGF and L. casei is more potent in protecting the barrier function from osmotic stress. These findings suggest that L. casei and EGF ameliorate osmotic stress-induced disruption of apical junctional complexes and barrier dysfunction in the intestinal epithelium by distinct signaling mechanisms. Full article

(This article belongs to the Special Issue EGF Receptor (EGFR) Trafficking Pathways: From Epithelial Cell Functions to Epithelial Carcinomas)

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Review

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15 pages, 1598 KiB

Open AccessReview

Epidermal Growth Factor Receptor Expression in the Corneal Epithelium

by Joanne L. Peterson and Brian P. Ceresa

Cells 2021, 10(9), 2409; https://doi.org/10.3390/cells10092409 - 13 Sep 2021

Cited by 16 | Viewed by 6092

Abstract

A properly functioning cornea is critical to clear vision and healthy eyes. As the most anterior portion of the eye, it plays an essential role in refracting light onto the retina and as an anatomical barrier to the environment. Proper vision requires that all layers be properly formed and fully intact. In this article, we discuss the role of the epidermal growth factor receptor (EGFR) in maintaining and restoring the outermost layer of the cornea, the epithelium. It has been known for some time that the addition of epidermal growth factor (EGF) promotes the restoration of the corneal epithelium and patients using EGFR inhibitors as anti-cancer therapies are at increased risk of corneal erosions. However, the use of EGF in the clinic has been limited by downregulation of the receptor. More recent advances in EGFR signaling and trafficking in corneal epithelial cells have provided new insights in how to overcome receptor desensitization. We examine new strategies for overcoming the limitations of high ligand and receptor expression that alter trafficking of the ligand:receptor complex to sustain receptor signaling. Full article

(This article belongs to the Special Issue EGF Receptor (EGFR) Trafficking Pathways: From Epithelial Cell Functions to Epithelial Carcinomas)

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