ArticleOncology reports2020
N‑glycosylation and receptor tyrosine kinase signaling affect claudin‑3 levels in colorectal cancer cells.
Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- N-Glycosylation of AXL Receptor Tyrosine Kinase Regulates Its Stability, Phosphorylation, and Oncogenic Function.Molecular & cellular proteomics : MCP · 2026Article
- ST6GAL1 promotes cancer stem-like cell-associated paclitaxel resistance through the EGFR-mTOR-SOX2/BMI1 axis in non-small cell lung cancer.Cancer drug resistance (Alhambra, Calif.) · 2026Article
- Immunoregulatory roles of post-translational modifications in colorectal cancer: mechanisms and therapeutic implications.Cellular and molecular life sciences : CMLS · 2025Review
- Article
- SARS-CoV-2, periodontal pathogens, and host factors: The trinity of oral post-acute sequelae of COVID-19.Reviews in medical virology · 2024Review
- Claudins in Cancer: A Current and Future Therapeutic Target.International journal of molecular sciences · 2024Review
- The Expression of the Claudin Family of Proteins in Colorectal Cancer.Biomolecules · 2024Review
- Analyzing aberrant DNA methylation in colorectal cancer uncovered intangible heterogeneity of gene effects in the survival time of patients.Scientific reports · 2023Article
- Identification of inflammatory factor-related genes associated with the prognosis and immune cell infiltration in colorectal cancer patients.Genes & diseases · 2023Article
- Aberrant N-glycosylation in cancer: MGAT5 and β1,6-GlcNAc branched N-glycans as critical regulators of tumor development and progression.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- C1GALT1 expression predicts a favorable prognosis and suppresses malignant phenotypes via TrkA signaling in neuroblastoma.Oncogenesis · 2022Article
- Evaluation of the Prognostic Relevance of Differential Claudin Gene Expression Highlights Claudin-4 as Being Suppressed by TGFβ1 Inhibitor in Colorectal Cancer.Frontiers in genetics · 2022Article
- Abnormal sialylation and fucosylation of saliva glycoproteins: Characteristics of lung cancer-specific biomarkers.Current research in pharmacology and drug discovery · 2022Review
- Effects of 1,2-Dimethylhydrazine on Barrier Properties of Rat Large Intestine and IPEC-J2 Cells.International journal of molecular sciences · 2021Article
- Pan-Cancer Analysis of CLDN3 and Its Contribution to 5-FU Resistance in Colorectal Cancer.IET systems biologyArticle
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in protein levels in different components of the apical junctional complex occur in colorectal cancer (CRC). Claudin‑3 is one of the main constituents of tight junctions, and its overexpression can increase the paracellular flux of macromolecules, as well as the malignant potential of CRC cells. The aim of this study was to investigate the molecular mechanisms involved in the regulation of claudin‑3 and its prognostic value in CRC. In silico evaluation in each of the CRC consensus molecular subtypes (CMSs) revealed that high expression levels of CLDN3 (gene encoding claudin‑3) in CMS2 and CMS3 worsened the patients' long‑term survival, whereas a decrease in claudin‑3 levels concomitant with a reduction in phosphorylation levels of epidermal growth factor receptor (EGFR) and insulin‑like growth factor 1 receptor (IGF1R) could be achieved by inhibiting N‑glycan biosynthesis in CRC cells. We also observed that specific inactivation of these receptor tyrosine kinases (RTKs) led to a decrease in claudin‑3 levels, and this regulation seems to be mediated by phospholipase C (PLC) and signal transducer and activator of transcription 3 (STAT3) in CRC cells. RTKs are modulated by their N‑linked glycans, and inhibition of N‑glycan biosynthesis decreased the claudin‑3 levels; therefore, we evaluated the correlation between N‑glycogenes and CLDN3 expression levels in each of the CRC molecular subtypes. The CMS1 (MSI immune) subtype concomitantly exhibited low expression levels of CLDN3 and N‑glycogenes (MGAT5, ST6GAL1, and B3GNT8), whereas CMS2 (canonical) exhibited high gene expression levels of CLDN3 and N‑glycogenes (ST6GAL1 and B3GNT8). A robust positive correlation was also observed between CLDN3 and B3GNT8 expression levels in all CMSs. These results support the hypothesis of a mechanism integrating RTK signaling and N‑glycosylation for the regulation of claudin‑3 levels in CRC, and they suggest that CLDN3 expression can be used to predict the prognosis of patients identified as CMS2 or CMS3.
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