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: closed (31 August 2024) | Viewed by 2390

Special Issue Editor


E-Mail
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
Special Issues, Collections and Topics in MDPI journals

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

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

  • cell adhesion
  • invasion
  • migration
  • extracellular matrix

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

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 - 6 Aug 2023
Cited by 2 | Viewed by 1958
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)
Show Figures

Figure 1

Back to TopTop