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Adhesion-Mediated Signaling during Cancer Progression
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Adhesion-Mediated Signaling during Cancer Progression

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 4688

Special Issue Editors

Prof. Dr. Avri Ben-Ze’ev

E-Mail Website
Guest Editor
Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
Interests: cell adhesion; cell motility; cancer progression; adhesion molecules; Wnt signaling; cancer stem cells; EMT; invasion and metastasis
Dr. Daniela Gabbia

E-Mail Website
Guest Editor
Department of Pharmaceutical and Pharmacological Sciences, University of Padova, L.go Meneghetti 2, 35131 Padova, Italy
Interests: chronic liver disease; hepatocellular carcinoma; liver metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cell adhesion to neighboring cells is a fundamental biological process in multicellular organisms that is required for tissue morphogenesis. A tight coordination between cell–cell adhesion, signaling, and gene expression is a characteristic feature of normal tissues. Changes, and often disruption of this coordination, are common during invasive and metastatic cancer development. This Special Issue on “Adhesion-Mediated Signaling during Cancer Progression” aims to collect studies that investigate the molecular intricacies involved in the changes in cell adhesion that promote the invasive and metastatic phenotype. The signaling pathways, the adhesion molecules, and possible stem cell and EMT signature genes that are involved in the process of invasive and metastatic cancer development are of interest for this issue.

Prof. Dr. Avri Ben-Ze’ev
Dr. Daniela Gabbia
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • cell adhesion
  • invasion
  • metastasis
  • cancer stem cells
  • EMT

Published Papers (3 papers)

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Research

19 pages, 3515 KiB  
Article
Plakophilin-3 Binds the Membrane and Filamentous Actin without Bundling F-Actin
by Jyoti Gupta, Erumbi S. Rangarajan, Regina B. Troyanovsky, Indrajyoti Indra, Sergey M. Troyanovsky and Tina Izard
Int. J. Mol. Sci. 2023, 24(11), 9458; https://doi.org/10.3390/ijms24119458 - 29 May 2023
Viewed by 1654
Abstract
Plakophilin-3 is a ubiquitously expressed protein found widely in epithelial cells and is a critical component of desmosomes. The plakophilin-3 carboxy-terminal domain harbors nine armadillo repeat motifs with largely unknown functions. Here, we report the 5 Å cryogenic electron microscopy (cryoEM) structure of [...] Read more.
Plakophilin-3 is a ubiquitously expressed protein found widely in epithelial cells and is a critical component of desmosomes. The plakophilin-3 carboxy-terminal domain harbors nine armadillo repeat motifs with largely unknown functions. Here, we report the 5 Å cryogenic electron microscopy (cryoEM) structure of the armadillo repeat motif domain of plakophilin-3, one of the smaller cryoEM structures reported to date. We find that this domain is a monomer or homodimer in solution. In addition, using an in vitro actin co-sedimentation assay, we show that the armadillo repeat domain of plakophilin-3 directly interacts with F-actin. This feature, through direct interactions with actin filaments, could be responsible for the observed association of extra-desmosomal plakophilin-3 with the actin cytoskeleton directly attached to the adherens junctions in A431 epithelial cells. Further, we demonstrate, through lipid binding analyses, that plakophilin-3 can effectively be recruited to the plasma membrane through phosphatidylinositol-4,5-bisphosphate-mediated interactions. Collectively, we report on novel properties of plakophilin-3, which may be conserved throughout the plakophilin protein family and may be behind the roles of these proteins in cell–cell adhesion. Full article
(This article belongs to the Special Issue Adhesion-Mediated Signaling during Cancer Progression)
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11 pages, 3316 KiB  
Article
Clinicopathological Significance of Cell Adhesion Molecule 4 Expression in Gallbladder Cancer and Its Prognostic Role
by Seongsik Bang, Seungyun Jee, Hwangkyu Son, Hyebin Cha, Kihyuk Song, Hosub Park, Jaekyung Myung, Hyunsung Kim and Seungsam Paik
Int. J. Mol. Sci. 2023, 24(8), 6898; https://doi.org/10.3390/ijms24086898 - 07 Apr 2023
Viewed by 1041
Abstract
Cell adhesion molecule 4 (CADM4) is involved in intercellular interactions and is a tumor-suppressor candidate. The role of CADM4 in gallbladder cancer (GBC) has not been reported. Therefore, the clinicopathological significance and prognostic value of CADM4 expression in GBC were evaluated in the [...] Read more.
Cell adhesion molecule 4 (CADM4) is involved in intercellular interactions and is a tumor-suppressor candidate. The role of CADM4 in gallbladder cancer (GBC) has not been reported. Therefore, the clinicopathological significance and prognostic value of CADM4 expression in GBC were evaluated in the present study. Immunohistochemistry (IHC) was performed on 100 GBC tissues to assess CADM4 expression at the protein level. The association between CADM4 expression and the clinicopathological characteristics of GBC was analyzed, and the prognostic significance of CADM4 expression was evaluated. Low CADM4 expression was significantly associated with advanced T category (p = 0.010) and high AJCC stage (p = 0.019). In a survival analysis, low CADM4 expression was associated with shorter overall survival (OS; p = 0.001) and recurrence-free survival (RFS; p = 0.018). In univariate analyses, low CADM4 expression was associated with shorter OS (p = 0.002) and RFS (p = 0.023). In multivariate analyses, low CADM4 expression was an independent prognostic factor of OS (p = 0.013). Low CADM4 expression was associated with tumor invasiveness and poor clinical outcomes in patients with GBC. CADM4 may play an important role in cancer progression and patient survival and can be used as a potential prognostic marker of GBC. Full article
(This article belongs to the Special Issue Adhesion-Mediated Signaling during Cancer Progression)
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14 pages, 4004 KiB  
Article
Artificial Intelligence-Based Computational Screening and Functional Assays Identify Candidate Small Molecule Antagonists of PTPmu-Dependent Adhesion
by Kathleen Molyneaux, Christian Laggner and Susann M. Brady-Kalnay
Int. J. Mol. Sci. 2023, 24(5), 4274; https://doi.org/10.3390/ijms24054274 - 21 Feb 2023
Cited by 2 | Viewed by 1403
Abstract
PTPmu (PTPµ) is a member of the receptor protein tyrosine phosphatase IIb family that participates in cell-cell adhesion and signaling. PTPmu is proteolytically downregulated in glioblastoma (glioma), and the resulting extracellular and intracellular fragments are believed to stimulate cancer cell growth and/or migration. [...] Read more.
PTPmu (PTPµ) is a member of the receptor protein tyrosine phosphatase IIb family that participates in cell-cell adhesion and signaling. PTPmu is proteolytically downregulated in glioblastoma (glioma), and the resulting extracellular and intracellular fragments are believed to stimulate cancer cell growth and/or migration. Therefore, drugs targeting these fragments may have therapeutic potential. Here, we used the AtomNet® platform, the first deep learning neural network for drug design and discovery, to screen a molecular library of several million compounds and identified 76 candidates predicted to interact with a groove between the MAM and Ig extracellular domains required for PTPmu-mediated cell adhesion. These candidates were screened in two cell-based assays: PTPmu-dependent aggregation of Sf9 cells and a tumor growth assay where glioma cells grow in three-dimensional spheres. Four compounds inhibited PTPmu-mediated aggregation of Sf9 cells, six compounds inhibited glioma sphere formation/growth, while two priority compounds were effective in both assays. The stronger of these two compounds inhibited PTPmu aggregation in Sf9 cells and inhibited glioma sphere formation down to 25 micromolar. Additionally, this compound was able to inhibit the aggregation of beads coated with an extracellular fragment of PTPmu, directly demonstrating an interaction. This compound presents an interesting starting point for the development of PTPmu-targeting agents for treating cancer including glioblastoma. Full article
(This article belongs to the Special Issue Adhesion-Mediated Signaling during Cancer Progression)
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