Epithelial cell adhesion molecule (EpCAM) is a glycoprotein on the surface of epithelial cells that is essential for intestinal epithelial integrity and expressed at high levels in many epithelial derived cancers and circulating tumor cells. Here we show the effect of EpCAM levels on migration of Madin-Darby-Canine Kidney (MDCK) epithelial cells. MDCK cells depleted of EpCAM show increased activation of extracellular signal-regulated kinase (ERK) and of myosin, and increased cell spreading and epithelial sheet migration into a gap. In contrast, over-expression of EpCAM inhibits ERK and myosin activation, and slows epithelial sheet migration. Loss of EpCAM is rescued by EpCAM-YFP mutated in the extracellular domain required for cis-dimerization whereas EpCAM-YFP with a mutation that inhibits Claudin-7 interaction cannot rescue increased ERK, myosin activation, and increased migration in EpCAM-depleted cells. In summary, these results indicate that interaction of EpCAM and Claudin-7 at the cell surface negatively regulates epithelial migration by inhibiting ERK and actomyosin contractility.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6179577 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0204957 | PLOS |
Publication Analysis
Top Keywords
Similar Publications
Sulforaphane inhibits TGF-β-induced fibrogenesis and inflammation in human Tenon's fibroblasts.
Mol Vis
November 2024
Department of Ophthalmology, the Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, PR China.
Purpose: Subconjunctival fibrosis is the main cause of failure after glaucoma filtration surgery. We explored the effects of sulforaphane (SFN) on the conversion of human Tenon's fibroblasts (HTFs) into myofibroblasts, transforming growth factor (TGF)-β-induced contraction of collagen gel, and inflammation.
Methods: After treatment with the combination of TGF-β and SFN or TGF-β alone, primary HTFs were subjected to a three-dimensional collagen contraction experiment to examine their contractility.
The alarmin, interleukin-33, increases vascular tone via extracellular signal regulated kinase-mediated Ca sensitization and endothelial nitric oxide synthase inhibition.
J Physiol
November 2024
Department of Physiology, Pharmacology & Toxicology, Health Sciences Center, West Virginia University, Morgantown, WV, USA.
Alarmins are classified by their release from damaged or ruptured cells. Many alarmins have been found to increase vascular tone and oppose endothelium-dependent dilatation (EDD). Interleukin (IL)-33 plays a prominent role in lung injury and can be released during vascular injury and in chronic studies found to be cardioprotective.
View Article and Find Full Text PDFInhibition of myotube formation by platelet-derived growth factor subunit B in QM7 cells.
Anim Biosci
January 2025
Department of Animal Science and Biotechnology, Kyungpook National University, Sangju 37224, Korea.
Objective: The primary objective of this study was to investigate the role and regulatory mechanisms of platelet-derived growth factor subunit B (PDGFB) in muscle differentiation.
Methods: In this study, a vector for PDGFB was designed and transfected into quail muscle cells to investigate its role and regulatory mechanism during muscle formation. To investigate the inhibitory mechanisms of PDGFB on myogenic differentiation, the mRNA expression levels of various genes and the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK 1/2), both known to regulate muscle development and differentiation were compared.
NLRX1 Mediates the Disruption of Intestinal Mucosal Function Caused by Porcine Astrovirus Infection via the Extracellular Regulated Protein Kinases/Myosin Light-Chain Kinase (ERK/MLCK) Pathway.
Cells
May 2024
Institute of Animal Husbandry and Veterinary Medicine, Shanghai Academy of Agricultural Sciences, Shanghai 201106, China.
() has a potential zoonotic risk, with a high proportion of co-infection occurring with () and other diarrheal pathogens. Despite its high prevalence, the cellular mechanism of pathogenesis is ill-defined. Previous proteomics analyses have revealed that the differentially expressed protein NOD-like receptor X1 (NLRX1) located in the mitochondria participates in several important antiviral signaling pathways in infection, which are closely related to mitophagy.
View Article and Find Full Text PDFCARMIL1 regulates liver cancer cell proliferation by activating the ERK/mTOR pathway through the TRIM27/p53 axis.
Int Immunopharmacol
June 2024
Department of Clinical Medicine, Guizhou Medical University, Guiyang, Guizhou, PR China; Department of Liver Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, PR China; Precision Medicine Research Institute of Guizhou, The Affiliated Hospital of Guizhou Medical University, Guiyang, PR China. Electronic address:
Article Synopsis
- CARMIL1 is a protein that plays a crucial role in forming actin networks and regulating cellular functions, particularly in liver cancer, where its effects on cell proliferation are being studied.
- Research indicates CARMIL1 promotes liver cancer cell growth by influencing key signaling pathways like ERK and mTOR, and its downregulation can affect their activity.
- The study found that inhibiting CARMIL1 increases liver cancer cells' sensitivity to the chemotherapy drug sorafenib, suggesting a potential treatment strategy that combines CARMIL1 suppression with sorafenib for better tumor control.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!