Evidence map›Paper›PMID 35169131›Full record

ArticleOncogenesis2022

C1GALT1 expression predicts a favorable prognosis and suppresses malignant phenotypes via TrkA signaling in neuroblastoma.

Neng-Yu Lin, Syue-Ting Chen, Hsiu-Ling Chang, Meng-Yao Lu, Yung-Li Yang, Shu-Wei Chou, Dong-Tsamn Lin, Kai-Hsin Lin, Shiann-Tarng Jou, Wen-Ming Hsu and 2 more

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Article in Oncogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Neng-Yu LinGraduate Institute of Anatomy and Cell Biology, National Taiwan University College of Medicine, Taipei, Taiwan.
Syue-Ting ChenGraduate Institute of Anatomy and Cell Biology, National Taiwan University College of Medicine, Taipei, Taiwan.
Hsiu-Ling ChangGraduate Institute of Anatomy and Cell Biology, National Taiwan University College of Medicine, Taipei, Taiwan.
Meng-Yao LuDepartment of Pediatrics, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.
Yung-Li YangDepartment of Pediatrics, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.
Shu-Wei ChouDepartment of Pediatrics, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.
Dong-Tsamn LinDepartment of Pediatrics, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.
Kai-Hsin LinDepartment of Pediatrics, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.
Shiann-Tarng JouDepartment of Pediatrics, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.
Wen-Ming HsuDepartment of Surgery, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.
Min-Chuan HuangGraduate Institute of Anatomy and Cell Biology, National Taiwan University College of Medicine, Taipei, Taiwan.ORCID http://orcid.org/0000-0002-0704-3447
Hsiu-Hao ChangDepartment of Pediatrics, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan. changhh2001@ntu.edu.tw.ORCID http://orcid.org/0000-0003-1832-8509
National Taiwan University Hospital · TWNational Taiwan University · TW

Funding

Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 108-2314-B-002-154Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 108-2320-B-002 -064 -MY3Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 109-2314-B-002-129Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 109-2320-B-002-039Ministry of Science and Technology, Taiwan (Ministry of Science and Technology of Taiwan) 110-2314-B-002-088-MY3National Taiwan University Hospital (NTUH) 108C101-83National Taiwan University Hospital (NTUH) 109C101-93National Taiwan University Hospital (NTUH) 111-S0028National Taiwan University Hospital (NTUH) NSCCMOH-131-92National Taiwan University Hospital (NTUH) NSCCMOH-94-8
6 · The paper itself

Abstract

Neuroblastoma (NB) is a childhood tumor derived from the sympathoadrenal lineage of the neural crest progenitor cells. Core 1 β1,3-galactosyltransferase (C1GALT1) controls the crucial step of GalNAc-type O-glycosylation, and its altered expression affects cancer behaviors. However, the role of C1GALT1 in NB tumors remains unclear. Our data showed that C1GALT1 expression was significantly associated with differentiated tumor histology, correlated with TrkA expression, and predicted good prognosis independently in NB. Downregulation of C1GALT1 promotes malignant behaviors of NB cells in vitro and in vivo. Mechanistic investigation showed that knockdown of C1GALT1 in NB cells increased TrkA pulled down through Vicia villosa agglutinin beads, indicating the modulation of O-glycans on TrkA by C1GALT1, and silencing C1GALT1 suppressed the TrkA expression on the NB cell surface. Overexpression of C1GALT1 increased the protein levels of TrkA and promoted the differentiation of NB cells, whereas knockdown of TrkA inhibited C1GALT1-induced neuronal differentiation. Moreover, the inhibitory effects of migration and invasion in C1GALT1-overexpressing NB cells were blocked by TrkA downregulation. C1GALT1 knockdown enhanced AKT phosphorylation but attenuated ERK phosphorylation, and these properties were consistent in C1GALT1-overexpressing NB cells with TrkA knockdown. Taken together, our data provided the first evidence for the existence of GalNAc-type O-glycans on TrkA and altered O-glycan structures by C1GALT1 can regulate TrkA signaling in NB cells. This study sheds light on the novel prognostic role of C1GALT1 in NB and provides new information of C1GALT1 and TrkA on the pathogenesis of NB.

Identifiers

PMID35169131
PMCPMC8847342
OpenAlexW4213187038

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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.