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Cells
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State of the Art in Integrin Signaling
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State of the Art in Integrin Signaling

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

Deadline for manuscript submissions: closed (15 March 2022) | Viewed by 7695

Special Issue Editor

Dr. Daniel Bouvard

E-Mail Website
Guest Editor
Centre de Recherche en Biologie Cellulaire- CNRS UMR5237, 919 Route de Mende, CEDEX 05, 34293 Montpellier, France
Interests: integrin signaling; mechanotransduction; bone formation; cell adhesion
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Integrin-mediated adhesions have long been recognized as the main molecular link attaching cells to the extracellular matrix (ECM). They are instrumental in bidirectional signaling and in informing the cell about the biophysical state of the ECM.

This Special Issue of Cells on “State of the Art in Integrin signaling” will broadly address how the ECM impacts cell fate and signaling through integrins, the importance of mechanotransduction in cell commitment and behavior, as well as the molecular basis of integrin and integrin-associated proteins in mechanosensing.

Consequently, we invite the community to submit original articles or reviews covering the above-mentioned field. Please ensure that your paper matches the scope of our journal. https://www.mdpi.com/journal/cells/about

We look forward to your contributions.

Dr. Daniel Bouvard
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

  • integrin
  • mechanotransduction
  • signaling
  • cell fate
  • ECM

Published Papers (3 papers)

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Research

16 pages, 5498 KiB  
Article
Integrin β3 Promotes Resistance to EGFR-TKI in Non-Small-Cell Lung Cancer by Upregulating AXL through the YAP Pathway
by Qi Sun, Zhihua Lu, Yanpeng Zhang, Dong Xue, Huayu Xia, Junjun She and Fanni Li
Cells 2022, 11(13), 2078; https://doi.org/10.3390/cells11132078 - 30 Jun 2022
Cited by 5 | Viewed by 2128
Abstract
Integrin β3 plays a key role in the resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI), but the development of integrin β3 inhibitors has been stalled due to the failure of phase III clinical trials for cancer treatment. Therefore, it is [...] Read more.
Integrin β3 plays a key role in the resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI), but the development of integrin β3 inhibitors has been stalled due to the failure of phase III clinical trials for cancer treatment. Therefore, it is imperative to find a potentially effective solution to the problem of acquired resistance to EGFR-TKI for patients with integrin-β3 positive non-small-cell lung cancer (NSCLC) by exploring novel downstream targets and action mechanisms of integrin β3. In the present study, we observed that the expression of integrin β3 and AXL was significantly upregulated in erlotinib-resistant NSCLC cell lines, which was further confirmed clinically in tumor specimens from patients with NSCLC who developed acquired resistance to erlotinib. Through ectopic expression or knockdown, we found that AXL expression was positively regulated by integrin β3. In addition, integrin β3 promoted erlotinib resistance in NSCLC cells by upregulating AXL expression. Furthermore, the YAP pathway, rather than pathways associated with ERK or AKT, was involved in the regulation of AXL by integrin β3. To investigate the clinical significance of this finding, the current well-known AXL inhibitor R428 was tested, demonstrating that R428 significantly inhibited resistance to erlotinib, colony formation, epithelial–mesenchymal transformation and cell migration induced by integrin β3. In conclusion, integrin β3 could promote resistance to EGFR-TKI in NSCLC by upregulating the expression of AXL through the YAP pathway. Patients with advanced NSCLC, who are positive for integrin β3, might benefit from a combination of AXL inhibitors and EGFR-TKI therapy. Full article
(This article belongs to the Special Issue State of the Art in Integrin Signaling)
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19 pages, 3477 KiB  
Article
Contribution of Endothelial Laminin-Binding Integrins to Cellular Processes Associated with Angiogenesis
by Hao Xu and Susan E. LaFlamme
Cells 2022, 11(5), 816; https://doi.org/10.3390/cells11050816 - 26 Feb 2022
Cited by 5 | Viewed by 2138
Abstract
Endothelial cells engage extracellular matrix and basement membrane components through integrin-mediated adhesion to promote angiogenesis. Angiogenesis involves the sprouting of endothelial cells from pre-existing vessels, their migration into surrounding tissue, the upregulation of angiogenesis-associated genes, and the formation of new endothelial tubes. To [...] Read more.
Endothelial cells engage extracellular matrix and basement membrane components through integrin-mediated adhesion to promote angiogenesis. Angiogenesis involves the sprouting of endothelial cells from pre-existing vessels, their migration into surrounding tissue, the upregulation of angiogenesis-associated genes, and the formation of new endothelial tubes. To determine whether the endothelial laminin-binding integrins, α6β4, and α3β1 contribute to these processes, we employed RNAi technology in organotypic angiogenesis assays, as well in migration assays, in vitro. The endothelial depletion of either α6β4 or α3β1 inhibited endothelial sprouting, indicating that these integrins have non-redundant roles in this process. Interestingly, these phenotypes were accompanied by overlapping and distinct changes in the expression of angiogenesis-associated genes. Lastly, depletion of α6β4, but not α3β1, inhibited migration. Taken together, these results suggest that laminin-binding integrins regulate processes associated with angiogenesis by distinct and overlapping mechanisms. Full article
(This article belongs to the Special Issue State of the Art in Integrin Signaling)
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33 pages, 5921 KiB  
Article
Overexpression and Activation of αvβ3 Integrin Differentially Affects TGFβ2 Signaling in Human Trabecular Meshwork Cells
by Mark S. Filla, Kristy K. Meyer, Jennifer A. Faralli and Donna M. Peters
Cells 2021, 10(8), 1923; https://doi.org/10.3390/cells10081923 - 29 Jul 2021
Cited by 14 | Viewed by 2780
Abstract
Studies from our laboratory have suggested that activation of αvβ3 integrin-mediated signaling could contribute to the fibrotic-like changes observed in primary open angle glaucoma (POAG) and glucocorticoid-induced glaucoma. To determine how αvβ3 integrin signaling could be involved in this process, RNA-Seq analysis was [...] Read more.
Studies from our laboratory have suggested that activation of αvβ3 integrin-mediated signaling could contribute to the fibrotic-like changes observed in primary open angle glaucoma (POAG) and glucocorticoid-induced glaucoma. To determine how αvβ3 integrin signaling could be involved in this process, RNA-Seq analysis was used to analyze the transcriptomes of immortalized trabecular meshwork (TM) cell lines overexpressing either a control vector or a wild type (WT) or a constitutively active (CA) αvβ3 integrin. Compared to control cells, hierarchical clustering, PANTHER pathway and protein-protein interaction (PPI) analysis of cells overexpressing WT-αvβ3 integrin or CA-αvβ3 integrin resulted in a significant differential expression of genes encoding for transcription factors, adhesion and cytoskeleton proteins, extracellular matrix (ECM) proteins, cytokines and GTPases. Cells overexpressing a CA-αvβ3 integrin also demonstrated an enrichment for genes encoding proteins found in TGFβ2, Wnt and cadherin signaling pathways all of which have been implicated in POAG pathogenesis. These changes were not observed in cells overexpressing WT-αvβ3 integrin. Our results suggest that activation of αvβ3 integrin signaling in TM cells could have significant impacts on TM function and POAG pathogenesis. Full article
(This article belongs to the Special Issue State of the Art in Integrin Signaling)
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