ArticleThe Journal of biological chemistry2013
N-glycosylation induces the CTHRC1 protein and drives oral cancer cell migration.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 79 citations in OpenAlex.
- LDHA Lactylation Drives Malignant Progression of Oral Squamous Cell Carcinoma via a Positive Feedback Loop with Lactate.International journal of biological sciences · 2026Article
- CTHRC1/TGF-β/Smad axis serves as therapeutic targets in inhibiting oral squamous cell carcinoma by mediating ferroptosis.Discover oncology · 2025Article
- Glycoproteomics of Gastrointestinal Cancers and Its Use in Clinical Diagnostics.Journal of proteome research · 2025Review
- In-situ profiling of glycosylation on single cells with surface plasmon resonance imaging.Nature communications · 2025Article
- CTHRC1: a key player in colorectal cancer progression and immune evasion.Frontiers in immunology · 2025Review
- WTAP promotes laryngeal carcinoma cell progression by posttranscriptional activation of CTHRC1 in an m6A-YTHDF1-dependent way.Cytotechnology · 2024Article
- CTHRC1 is a prognostic biomarker correlated with immune infiltration in head and neck squamous cell carcinoma.BMC oral health · 2024Article
- Review
- The role of collagen triple helix repeat containing 1 (CTHRC1) in cancer development and progression.Expert opinion on therapeutic targets · 2024Review
- B4GALT1 promotes immune escape by regulating the expression of PD-L1 at multiple levels in lung adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2023Article
- CTHRC1, a novel gene with multiple functions in physiology, disease and solid tumors (Review).Oncology letters · 2023Review
- CTHRC1 is associated with immune cell infiltration and functions as an adverse marker for prognosis in head and neck squamous cell carcinoma.Oncology letters · 2023Article
- CTHRC1 facilitates bladder cancer cell proliferation and invasion through regulating the PI3K/Akt signaling pathway.Archives of medical science : AMS · 2022Article
- The molecular mechanisms of CTHRC1 in gastric cancer by integrating TCGA, GEO and GSA datasets.Frontiers in genetics · 2022Article
- Comprehensive Analysis of the Potential Prognostic Value of 11 Glycosylation-Related Genes in Head and Neck Squamous Cell Carcinoma and Their Correlation with PD-L1 Expression and Immune Infiltration.Journal of oncology · 2022Article
- Article
- Pan-cancer analysis combined with experiments predicts CTHRC1 as a therapeutic target for human cancers.Cancer cell international · 2021Article
- Epithelial-Mesenchymal Transition Associated with Head and Neck Squamous Cell Carcinomas: A Review.Cancers · 2021Review
- Novel deep learning-based survival prediction for oral cancer by analyzing tumor-infiltrating lymphocyte profiles through CIBERSORT.Oncoimmunology · 2021Article
- The Role of Collagen Triple Helix Repeat-Containing 1 Protein (CTHRC1) in Rheumatoid Arthritis.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Oral squamous cell carcinoma (OSCC) is one of the most pernicious malignancies, but the mechanisms underlying its development and progression are poorly understood. One of the key pathways implicated in OSCC is the canonical Wnt/β-catenin signaling pathway. Previously, we reported that canonical Wnt signaling functions in a positive feedback loop with the DPAGT1 gene, a principal regulator of the metabolic pathway of protein N-glycosylation, to hyperglycosylate E-cadherin and reduce intercellular adhesion. Here, we show that in OSCC, DPAGT1 and canonical Wnt signaling converge to up-regulate CTHRC1 (collagen triple helix repeat containing 1), an N-glycoprotein implicated in tumor invasion and metastasis. We found that in human OSCC specimens, amplification of the levels of CTHRC1 was associated with its hyperglycosylation. Partial inhibition of DPAGT1 expression in OSCC CAL27 cells reduced CTHRC1 abundance by increasing protein turnover, indicating that N-glycosylation stabilizes CTHRC1. Additionally, canonical Wnt signaling promoted β-catenin/T-cell factor transcriptional activity at the CTHRC1 promoter to further elevate CTHRC1 levels. We demonstrate that DPAGT1 promotes cell migration and drives the localization of CTHRC1 to cells at the leading edge of a wound front coincident with drastic changes in cell morphology. We propose that in OSCC, dysregulation of canonical Wnt signaling and DPAGT1-dependent N-glycosylation induces CTHRC1, thereby driving OSCC cell migration and tumor spread.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.