Evidence map›Paper›PMID 29930379›Full record

ArticleOncogene2018

C1GALT1 predicts poor prognosis and is a potential therapeutic target in head and neck cancer.

Mei-Chun Lin, Pin-Hui Chien, Hsin-Yi Wu, Syue-Ting Chen, Hsueh-Fen Juan, Pei-Jen Lou, Min-Chuan Huang

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
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  10. Glycosylation in Cancer.Handbook of experimental pharmacology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Mei-Chun LinDepartment of Otolaryngology, National Taiwan University Hospital, Hsin-Chu Branch, Hsinchu, Taiwan.
Pin-Hui ChienDepartment of Otolaryngology, National Taiwan University Hospital, Hsin-Chu Branch, Hsinchu, Taiwan.
Hsin-Yi WuInstrumentation Center, National Taiwan University, Taipei, Taiwan.
Syue-Ting ChenGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Hsueh-Fen JuanDepartment of Life Science, Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University, Taipei, Taiwan.
Pei-Jen LouDepartment of Otolaryngology, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan. pjlou@ntu.edu.tw.
Min-Chuan HuangGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan. mchuang@ntu.edu.tw.
National Taiwan University · TWNational Taiwan University Hospital · TW

Funding

Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 103-2314-B-002 -082 -MY2Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 104-2320-B-002 -068 -MY3Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 105-2314-B-002 -203 -MY2
6 · The paper itself

Abstract

Core 1 β1,3-galactosyltransferase (C1GALT1) controls the crucial step of GalNAc-type O-glycosylation and is overexpressed in various human malignancies. However, its role in head and neck squamous cell carcinoma (HNSCC) remains unclear. Here we demonstrate that C1GALT1 expression is upregulated in HNSCC tumors and is associated with adverse clinicopathologic features. Moreover, high C1GALT1 expression predicts poor disease-free and overall survivals. C1GALT1 overexpression enhances HNSCC cell viability, migration, and invasion, which can be reversed by erlotinib. Silencing of C1GALT1 suppresses the malignant behavior both in vitro and in vivo. Mass spectrometry and lectin pull-down assays demonstrate that C1GALT1 modifies O-glycans on EGFR. Blocking O-glycan elongation on EGFR by C1GALT1 knockdown decreases EGF-EGFR binding affinity and inhibits EGFR signaling, thereby suppressing malignant phenotypes. Using molecular docking simulations, we identify itraconazole as a C1GALT1 inhibitor that directly binds C1GALT1 and promotes its proteasomal degradation, leading to significant blockade of C1GALT1-mediated effects in HNSCC cells in vitro and in vivo. Collectively, our findings demonstrate a critical role of O-glycosylation in HNSCC progression and highlight the therapeutic potential of targeting C1GALT1 in HNSCC treatment.

Indexed as

Cell MovementGalactosyltransferasesGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticItraconazoleMolecular Docking SimulationNeoplasm ProteinsCell Line, TumorCell SurvivalErbB ReceptorsFemaleGlycosylationHead and Neck NeoplasmsHumansMaleNeoplasm InvasivenessC1GALT1 protein, humanEGFR protein, humanErbB ReceptorsGalactosyltransferasesItraconazoleNeoplasm Proteins

Identifiers

PMID29930379
PMCPMC6202324
OpenAlexW2809339027

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.