Evidence map›Paper›PMID 37479744›Full record

ArticleCell death and differentiation2023

Targeting N-glycosylation of 4F2hc mediated by glycosyltransferase B3GNT3 sensitizes ferroptosis of pancreatic ductal adenocarcinoma.

Heng Ma, Xianlong Chen, Shengwei Mo, Yue Zhang, Xinxin Mao, Jingci Chen, Yilin Liu, Wei-Min Tong, Zhaohui Lu, Shuangni Yu and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
11.4field-weighted citation impact, top 1% 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

37 citing papers in PubMed, 44 citations in OpenAlex.

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  20. The Intersection of Glycosylation and Ferroptosis in Cancer.Antioxidants (Basel, Switzerland) · 2025
    Review
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

11 authors at 1 institution in 1 country.

Heng MaDepartment of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China.ORCID 0000-0002-8729-8430
Xianlong ChenDepartment of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China.ORCID 0000-0002-3677-4281
Shengwei MoDepartment of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China.ORCID 0000-0001-9401-3141
Yue ZhangDepartment of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China.ORCID 0000-0002-8553-708X
Xinxin MaoDepartment of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China.
Jingci ChenDepartment of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China.ORCID 0000-0002-2349-3309
Yilin LiuDepartment of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China.ORCID 0000-0001-8908-6194
Wei-Min TongDepartment of Pathology, Institute of Basic Medical Sciences, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China.ORCID 0000-0002-6240-0267
Zhaohui LuDepartment of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China.ORCID 0000-0002-8421-7033
Shuangni YuDepartment of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China. yushn@pumch.cn.ORCID 0000-0002-3745-1097
Jie ChenDepartment of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Science, Beijing, 100730, China. chenjie@pumch.cn.ORCID 0000-0002-2658-9525
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) remains a highly fatal malignancy partially due to the acquired alterations related to aberrant protein glycosylation that pathologically remodel molecular biological processes and protect PDAC cells from death. Ferroptosis driven by lethal lipid peroxidation provides a targetable vulnerability for PDAC. However, the crosstalk between glycosylation and ferroptosis remains unclear. Here, we identified 4F2hc, a subunit of the glutamate-cystine antiporter system X

Indexed as

Carcinoma, Pancreatic DuctalFerroptosisPancreatic NeoplasmsCell Line, TumorGlycosylationGlycosyltransferasesHumansN-AcetylglucosaminyltransferasesB3GNT3 protein, humanGlycosyltransferasesN-Acetylglucosaminyltransferases

Identifiers

PMID37479744
PMCPMC10406883
OpenAlexW4385064667

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.