Cell-cell adhesion molecules (CAMs) comprise a broad class of linker proteins that are crucial for the development of multicellular organisms, and for the continued maintenance of organ and tissue structure. Because of its pivotal function in tissue homeostasis, the deregulation of intercellular adhesion is linked to the onset of most solid tumors. The breakdown of homeostatic cell adhesions in highly ordered epithelial sheets is directly implicated in carcinogenesis, while continued changes in the adhesion profile of the primary tumor mass facilitate growth and expansion into adjacent tissue. Intercellular adhesion molecules are also involved in each subsequent phase of metastasis, including transendothelial migration, transit through the bloodstream or lymphatics, and renewed proliferation in secondary sites. This review addresses various roles of cadherin- and selectin-mediated intercellular adhesion in tumor initiation and malignant transformation, and discusses the mechanisms for the arrest and adhesion of circulating tumor cells to the vessel endothelium. Considering the contributions of these CAMs to cancer progression in the context of a systematic biological framework may prove valuable in identifying new ways to diagnose and treat cancer.
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http://dx.doi.org/10.1002/wsbm.160 | DOI Listing |
Sci Rep
January 2025
Department of Biomedical Engineering, University of Rochester, Rochester, NY, USA.
The aberrant vascular response associated with tendon injury results in circulating immune cell infiltration and a chronic inflammatory feedback loop leading to poor healing outcomes. Studying this dysregulated tendon repair response in human pathophysiology has been historically challenging due to the reliance on animal models. To address this, our group developed the human tendon-on-a-chip (hToC) to model cellular interactions in the injured tendon microenvironment; however, this model lacked the key element of physiological flow in the vascular compartment.
View Article and Find Full Text PDFInflamm Res
January 2025
Departamento de Biomedicina - Unidade de Farmacologia e Terapêutica, Faculdade de Medicina da Universidade do Porto (FMUP), Rua Dr. Plácido da Costa, S/N, Edifício Poente, Piso 3, 4200-450, Porto, Portugal.
Background And Aims: Endocan has been scarcely explored in COVID-19, especially regarding its modulation by veno-venous extracorporeal membrane oxygenation (VV-ECMO), hypertension or previous renin-angiotensin-aldosterone system (RAAS) inhibitors treatment. We compared endocan and other endotheliitis markers in hospitalized COVID-19 patients and assessed their modulation by VV-ECMO, hypertension and previous RAAS inhibitors treatment.
Material And Methods: Serum endocan, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin were measured in "severe" (n = 27), "critically ill" (n = 17) and "critically ill on VV-ECMO" (n = 17) COVID-19 patients at admission, days 3-4, 5-8 and weekly thereafter, and in controls (n = 23) at a single time point.
Int J Mol Sci
January 2025
Department of Oncology, University of Torino, 10060 Candiolo, Italy.
Tumor-associated macrophages (TAMs) are one of the most abundant cell types in the colorectal cancer (CRC) tumor microenvironment (TME). CRC cell-derived exosomes support macrophage polarization toward an M2-like phenotype, which leads to tumor growth and metastasis. Neuroligin 1 (NLG1) is a transmembrane protein critical in synaptic function.
View Article and Find Full Text PDFBiomolecules
December 2024
Department of Pharmacology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Upon exposure to inflammatory stimuli including TNF-α, endothelial cells are activated leading to the adhesion of monocytes to their surface. These events are involved in the pathophysiology of atherosclerosis. Since TNF-α activates the NF-κB pathway, which contributes to atherosclerosis, targeting this signaling pathway may help prevent the risk of developing the disease.
View Article and Find Full Text PDFBiomolecules
December 2024
Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, 140 21 Prague, Czech Republic.
We investigated the sex-dependent effects of inflammatory responses in visceral adipose tissue (VAT) and perivascular adipose tissue (PVAT), as well as hematological status, in relation to cardiovascular disorders associated with prediabetes. Using male and female hereditary hypertriglyceridemic (HHTg) rats-a nonobese prediabetic model featuring dyslipidemia, hepatic steatosis, and insulin resistance-we found that HHTg females exhibited more pronounced hypertriglyceridemia than males, while HHTg males had higher non-fasting glucose levels. Additionally, HHTg females had higher platelet counts, larger platelet volumes, and lower antithrombin inhibitory activity.
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