The epithelial lateral membrane plays a central role in the integration of intercellular signals and, by doing so, is a principal determinant in the emerging properties of epithelial tissues. Mechanical force, when applied to the lateral cell-cell interface, can modulate the strength of adhesion and influence intercellular dynamics. Yet the relationship between mechanical force and epithelial cell behavior is complex and not completely understood. This commentary aims to provide an investigative look at the usage of cellular forces at the epithelial cell-cell adhesion interface.
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http://dx.doi.org/10.12688/f1000research.15860.1 | DOI Listing |
BMC Med Genomics
January 2025
Department of Surgery, Faculty of General of Medicine, Koya University, Koya, Kurdistan Region - F.R., KOY45, Iraq.
Background: During mammalian spermatogenesis, the cytoskeleton system plays a significant role in morphological changes. Male infertility such as non-obstructive azoospermia (NOA) might be explained by studies of the cytoskeletal system during spermatogenesis.
Methods: The cytoskeleton, scaffold, and actin-binding genes were analyzed by microarray and bioinformatics (771 spermatogenic cellsgenes and 774 Sertoli cell genes).
Cells Dev
January 2025
Quantitative and Imaging Biology, International Research Collaboration Center (IRCC), National Institutes of Natural Sciences (NINS), Japan; Trans-Scale Biology Center, National Institute for Basic Biology (NIBB), National Institutes of Natural Sciences (NINS), Japan. Electronic address:
Collective cell migration is a fundamental process underlying various biological phenomena, including embryonic development and cancer cell invasion. The cohesive yet flexible movement of cell collectives largely depends on the coordinated regulation of cell-cell and cell-substrate adhesions. In this review, we summarize the regulation of key cell-cell junction components, such as cadherins and zonula occludens proteins during collective cell migration, with a particular focus on the recently discovered multifaceted roles of ZO-1 in both cell-cell and cell-substrate interactions.
View Article and Find Full Text PDFNeoplasia
January 2025
Department of Gynecology and Obstetrics, Technical University of Munich, 81675 Munich, Germany; German Cancer Consortium (DKTK), partner site Munich, and German Cancer Research Center (DKFZ), Heidelberg, Germany. Electronic address:
T-cell recruiting chemokines are required for a successful immune intervention in ovarian cancer, and also for the efficacy of modern anticancer agents such as PARP inhibitors. The chemokine CX3CL1 recruits tumour-suppressive T-cells into solid tumours, but also mediates cell-cell adhesions, e.g.
View Article and Find Full Text PDFNat Med
January 2025
Department of Biology, Institute of Molecular Health Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland.
The presence of circulating tumor cell (CTC) clusters is associated with disease progression and reduced survival in a variety of cancer types. In breast cancer, preclinical studies showed that inhibitors of the Na/K ATPase suppress CTC clusters and block metastasis. Here we conducted a prospective, open-label, proof-of-concept study in women with metastatic breast cancer, where the primary objective was to determine whether treatment with the Na/K ATPase inhibitor digoxin could reduce mean CTC cluster size.
View Article and Find Full Text PDFFront Immunol
January 2025
Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, United States.
Cluster of Differentiation 6 (CD6), an established marker of T cells, has multiple and complex functions in regulation of T cell activation and proliferation, and in adhesion of T cells to antigen-presenting cells and epithelial cells in various organs and tissues. Early studies on CD6 demonstrated its role in mediating cell-cell interactions through its first ligand to be identified, CD166/ALCAM. The observation of CD6-dependent functions of T cells that could not be explained by interactions with CD166/ALCAM led to discovery of a second ligand, CD318/CDCP1.
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