AI Article Synopsis
- * Researchers used various techniques, such as bioinformatics and Western blotting, to show that CDH5 levels are higher in gastric cancer tissues and correlate with worse patient outcomes.
- * The findings suggest that Notch1 activates CDH5, promoting cancer cell proliferation and migration, so targeting this pathway could offer new treatment options for gastric cancer.
Article Abstract
Objective: To explore the underlying molecular mechanism of Notch1/cadherin 5 (CDH5) pathway in modulating in cell malignant behaviors of gastric cancer (GC).
Methods: We performed bioinformatic analyses to screen the potential target genes of Notch1 from cadherins in GC. Western blot and RT-PCR were conducted to detect CDH5 expression in GC tissues and cells. We utilized chromatin immunoprecipitation (CHIP) assays to assess the interaction of Notch1 with CDH5 gene. The effects of Notch1/CDH5 axis on the proliferation, invasion, migration and vasculogenic mimicry in GC cells were evaluated by EdU, wound healing, transwell, and tubule formation assays.
Results: Significantly increased CDH5 expression was found in GC tissues compared with paracancerous tissues and associated to clinical stage and poor overall survival (OS) in patients with GC. Notch1 positively regulate the expression of CDH5 in GC cells. CHIP assays validated that CDH5 was a direct target of Notch1. In addition, Notch1 upregulation enhanced the proliferation, migration, invasion and vasculogenic mimicry capacity of GC cells, which could be attenuated by CDH5 silencing.
Conclusions: These results indicated Notch1 upregulation enhanced GC malignant behaviors by triggering CDH5, suggesting that targeting Notch1/CDH5 axis could be a potential therapeutic strategy for GC progression.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11386911 | PMC |
| http://dx.doi.org/10.18632/aging.206061 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Extracranial arteriovenous malformations (eAVMs) are complex vascular lesions characterized by anomalous arteriovenous connections, vascular instability, and disruptions in endothelial cell (EC)-to-mural cell (MC) interactions. This study sought to determine whether eAVM-MCs could induce endothelial-to-mesenchymal transition (EndMT), a process known to disrupt vascular integrity, in the eAVM microenvironment. eAVM and paired control tissues were analyzed using RT-PCR for EC (, , and ) and EndMT-specific markers (, , , /.
View Article and Find Full Text PDFFlow-Dependent Modulation of Endothelial Ca Dynamics by Small Conductance Ca-Activated K Channels in Mouse Carotid Arteries.
Biomedicines
December 2024
Department of Physiology and Cell Biology, University of South Alabama College of Medicine, Mobile, AL 36688, USA.
Background: Small conductance Ca activated K channels (K2.3) are important regulators of vascular function. They provide Ca-dependent hyperpolarization of the endothelial membrane potential, promoting agonist-induced vasodilation.
View Article and Find Full Text PDFArticle Synopsis
- Gastric cancer has a poor prognosis and varied cellular characteristics, highlighting the need for a better understanding of its tumor microenvironment and heterogeneity to create effective treatments.
- Researchers analyzed single-cell RNA sequencing data and used machine learning to identify 18 significant genes related to gastric cancer, with a particular focus on NFKBIE, which showed a strong correlation with patient risk levels.
- The study suggests NFKBIE could serve as a potential biomarker and therapeutic target, with certain drugs like gemcitabine and chloropyramine possibly being effective against high-risk gastric cancer patients.
FYN regulates aqueous humor outflow and IOP through the phosphorylation of VE-CADHERIN.
Nat Commun
January 2025
Department of Ophthalmology, Columbia University Irving Medical Center, New York, NY, USA.
Schlemm's canal endothelial cells (SECs) serve as the final barrier to aqueous humor (AQH) drainage from the eye. SECs adjust permeability to AQH outflow to modulate intraocular pressure (IOP). The broad identification of IOP-related genes implicates SECs in glaucoma.
View Article and Find Full Text PDFAKT1-Mediated NOTCH1 phosphorylation promotes gastric cancer progression via targeted regulation of IRS-1 transcription.
J Cancer Res Clin Oncol
December 2024
The First Clinical Medical College, Lanzhou University, Lanzhou, 730000, China.
Purpose: This study aimed to investigate that AKT1-Mediated NOTCH1 phosphorylation promotes gastric cancer (GC) progression via targeted regulation of IRS-1 transcription.
Methods: The study utilized databases such as PhosphositePlus, TRANSFAC, CHEA, GPS 5.0, and TCGA, along with experimental techniques including Western Blot, co-IP, in vitro kinase assay, construction of lentiviral overexpression and silencing vectors, immunoprecipitation, modified proteomics, immunofluorescence, ChIP-PCR, EdU assay, Transwell assay, and scratch assay to investigate the effects of AKT1-induced Notch1 phosphorylation on cell proliferation, invasion and migration in vitro, as well as growth and epithelial-mesenchymal transition (EMT) in vivo.
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!