Evidence map›Paper›PMID 31827081›Full record

ArticleCell death & disease2019

Transcription factor NFAT5 contributes to the glycolytic phenotype rewiring and pancreatic cancer progression via transcription of PGK1.

Yongsheng Jiang, Ruizhe He, Yuhong Jiang, Dejun Liu, Lingye Tao, Minwei Yang, Chaoyi Lin, Yang Shen, Xueliang Fu, Jianyu Yang and 8 more

Abstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
–field-weighted citation impact
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

47 citing papers in PubMed.

  1. Review
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  5. Heavy metal-induced disruption of the autophagy-lysosomal pathway: implications for aging and neurodegenerative disorders.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025
    Review
  6. [Expression of NFAT5 and IGF1R in nasopharyngeal carcinoma tissues and analysis of clinical characteristics].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2025
    Article
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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

18 authors.

Yongsheng JiangDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Ruizhe HeDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Yuhong JiangQingdao Women and Children's Hospital, Qingdao, China.
Dejun LiuDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Lingye TaoDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Minwei YangDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Chaoyi LinDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Yang ShenDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Xueliang FuDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.ORCID http://orcid.org/0000-0002-2454-207X
Jianyu YangDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Jiao LiDepartment of Hepatobiliary Pancreas Surgery, Shanghai East Hospital, Tong Ji University School of Medicine, Shanghai, P. R. China.
Yanmiao HuoDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Rong HuaDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Wei LiuDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Junfeng ZhangDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China.
Baiyong ShenDepartment of General Surgery, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China. shenby@shsmu.edu.cn.
Zhigang ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China. zzhang@shsci.org.ORCID http://orcid.org/0000-0001-8965-223X
Yongwei SunDepartment of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P. R. China. syw0616@126.com.ORCID http://orcid.org/0000-0002-5937-634X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81672358National Natural Science Foundation of China (National Science Foundation of China) Project 81502489National Natural Science Foundation of China (National Science Foundation of China) Project 81802317
6 · The paper itself

Abstract

Hypoxia and the hypovascular tumor microenvironment are major hallmarks of pancreatic ductal adenocarcinoma (PDAC), in which glycolysis is of great importance to tumor survival and proliferation. There is little research regarding the role of Nuclear Factor of Activated T Cells 5 (NFAT5) in relation to carcinoma. Here, we explored the impact of NFAT5 on the biological behavior of PDAC and the underlying mechanism. We demonstrated that NFAT5 was highly expressed in PDAC and was related to poorer prognosis. Knockdown of NFAT5 lead to impaired proliferation of tumor cells caused by an aberrant Warburg effect. Mechanically, phosphoglycerate kinase 1 (PGK-1), which is the first enzyme generating ATP in glycolysis, was verified as a target gene of NFAT5. Over-expression of PGK1 compromised the aberrant oncological behavior caused by knockdown of NFAT5 both in vitro and in vivo. Clinical samples underwent positron emission tomography-computed tomography (PET-CT) examination and KrasG12D/+/Trp53R172H/+/Pdx1-Cre (KPC) mice were collected to support our conclusion.

Indexed as

Transcription, GeneticAdenocarcinomaAgedAnimalsCarcinoma, Pancreatic DuctalCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticGlycolysisHeterograftsHomeodomain ProteinsHumansMaleMiceMiddle AgedHomeodomain ProteinsKRAS protein, humanNFAT5 protein, humanpancreatic and duodenal homeobox 1 proteinPGK1 protein, humanPhosphoglycerate KinaseProto-Oncogene Proteins p21(ras)TP53 protein, humanTrans-ActivatorsTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID31827081
PMCPMC6906509

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Registered trials

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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.