Cell Adhesion/Migration in Tumor Metastasis

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

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1760

Special Issue Editor


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Guest Editor
CNRS UMR 5237, Centre de Recherche en Biologie Cellulaire de Montpellier (CRBM), Université de Montpellier, Montpellier, France
Interests: cell adhesion; integrin; late endosomes; cell signaling; hippo pathway; osteoblast; bone
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Special Issue Information

Dear Colleagues,

Cell migration plays a critical role in many physio-pathological processes, including cancer progression. Tumour metastasis is a deadly consequence of tumour cell invasion and dissemination. In addition, 2D cell migration in specific extracellular matrixes typically relies on the formation of protrusions, mechanosensitive cell attachment to the ECM, actin-based force generation to propel cell movement and finally, adhesion disassembly at the cell rear. Following the in-depth study of the key steps of the process, new regulatory pathways and accessory proteins are emerging. At the same time, the availability of new tools to address how the cells move in a 3D environment is adding to the complexity of how this coordinated event has to be regulated. The aim of this Special Issue is to compile original and review articles that deal with cell invasion and migration in 2D as well as 3D. Work that presents new innovative technical approaches or protein functions related to this process is very welcome.

Dr. Daniel Bouvard
Guest Editor

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Keywords

  • cell adhesion
  • invasion
  • migration
  • extracellular matrix

Published Papers (1 paper)

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Research

15 pages, 2280 KiB  
Article
GSK-J4 Inhibition of KDM6B Histone Demethylase Blocks Adhesion of Mantle Cell Lymphoma Cells to Stromal Cells by Modulating NF-κB Signaling
by Laia Sadeghi and Anthony P. H. Wright
Cells 2023, 12(15), 2010; https://doi.org/10.3390/cells12152010 - 06 Aug 2023
Cited by 1 | Viewed by 1472
Abstract
Multiple signaling pathways facilitate the survival and drug resistance of malignant B-cells by regulating their migration and adhesion to microenvironmental niches. NF-κB pathways are commonly dysregulated in mantle cell lymphoma (MCL), but the exact underlying mechanisms are not well understood. Here, using a [...] Read more.
Multiple signaling pathways facilitate the survival and drug resistance of malignant B-cells by regulating their migration and adhesion to microenvironmental niches. NF-κB pathways are commonly dysregulated in mantle cell lymphoma (MCL), but the exact underlying mechanisms are not well understood. Here, using a co-culture model system, we show that the adhesion of MCL cells to stromal cells is associated with elevated levels of KDM6B histone demethylase mRNA in adherent cells. The inhibition of KDM6B activity, using either a selective inhibitor (GSK-J4) or siRNA-mediated knockdown, reduces MCL adhesion to stromal cells. We showed that KDM6B is required both for the removal of repressive chromatin marks (H3K27me3) at the promoter region of NF-κB encoding genes and for inducing the expression of NF-κB genes in adherent MCL cells. GSK-J4 reduced protein levels of the RELA NF-κB subunit and impaired its nuclear localization. We further demonstrated that some adhesion-induced target genes require both induced NF-κB and KDM6B activity for their induction (e.g., IL-10 cytokine gene), while others require induction of NF-κB but not KDM6B (e.g., CCR7 chemokine gene). In conclusion, KDM6B induces the NF-κB pathway at different levels in MCL, thereby facilitating MCL cell adhesion, survival, and drug resistance. KDM6B represents a novel potential therapeutic target for MCL. Full article
(This article belongs to the Special Issue Cell Adhesion/Migration in Tumor Metastasis)
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