Evidence map›Paper›PMID 32114387›Full record

ArticleEBioMedicine2020

Orphan nuclear receptor Nurr1 promotes Helicobacter pylori-associated gastric carcinogenesis by directly enhancing CDK4 expression.

Wenjing Shang, Xiuming Liang, Shuyan Li, Tongyu Li, Lixin Zheng, Wei Shao, Yue Wang, Fen Liu, Lin Ma, Jihui Jia

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Advances inOncology letters · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. International journal of biological sciences · 2024
    Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Diagnostic approach toAnnals of gastroenterology
    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

10 authors at 1 institution in 1 country.

Wenjing ShangDepartment of Microbiology/Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China; Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China.
Xiuming LiangDepartment of Microbiology/Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China; Shandong University-Karolinska Institute Collaborative Laboratory for Cancer Research, Jinan, Shandong 250012, PR China.
Shuyan LiDepartment of Microbiology/Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China.
Tongyu LiDepartment of Microbiology/Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China.
Lixin ZhengDepartment of Microbiology/Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China.
Wei ShaoDepartment of Microbiology/Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China.
Yue WangDepartment of Microbiology/Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China.
Fen LiuDepartment of Microbiology/Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China.
Lin MaDepartment of Microbiology/Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China; Qianfoshan Hospital, Jinan, Shandong 250012, PR China. Electronic address: 2375@sdhospital.com.cn.
Jihui JiaDepartment of Microbiology/Key Laboratory for Experimental Teratology of the Chinese Ministry of Education, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China; Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Science, Shandong University, Jinan, Shandong 250012, PR China; Shandong University-Karolinska Institute Collaborative Laboratory for Cancer Research, Jinan, Shandong 250012, PR China. Electronic address: jiajihui@sdu.edu.cn.
Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAbnormal expression of the orphan nuclear receptor Nurr1 is a critical factor in the etiology of multiple cancers. However, its potential role in gastric cancer (GC) remains elusive. In this study, we have demonstrated that the expression of Nurr1 was elevated and had an oncogenic function in GC.

methodsNurr1 expression was analyzed in clinical specimens and the GEO database. Functions of Nurr1 in GC cells were analyzed using Nurr1 knockdown and overexpression. Various cell and molecular biological methods were used to explore the potential mechanisms of Nurr1 upregulation and its role in promoting GC.

findingsOverexpression of Nurr1 was directly related to the poor prognosis of GC patients. What's more, Nurr1 was induced by Helicobacter pylori (H. pylori) via the PI3K/AKT-Sp1 pathway. Sp1 enhanced Nurr1 expression by binding to its promoter to activate the transcription. Upregulated Nurr1 then directly targeted CDK4 by binding to its promoter region to increase its expression, thereby facilitated GC cells proliferation both in vitro and in vivo.

interpretationWe identified Nurr1 as a driving oncogenic factor in GC. In addition, Nurr1 could be used as a potential therapeutic target for the diagnosis and treatment of H. pylori-associated GC.

fundingThis work was supported by the National Natural Science Foundation of China (Nos 81801983, 81871620, 81971901, 81772151 and 81571960), and the Department of Science and Technology of Shandong Province (2018CXGC1208).

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinogenesisCell Line, TumorCyclin-Dependent Kinase 4Helicobacter pyloriHumansMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, NudeNuclear Receptor Subfamily 4, Group A, Member 2Phosphatidylinositol 3-KinasesPromoter Regions, GeneticProto-Oncogene Proteins c-aktCDK4 protein, humanCyclin-Dependent Kinase 4NR4A2 protein, humanNuclear Receptor Subfamily 4, Group A, Member 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSp1 Transcription FactorCDK4Gastric cancerHelicobacter pyloriPI3K/AKT/Sp1Proliferation

Identifiers

PMID32114387
PMCPMC7047206
OpenAlexW3007885244

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.