Evidence map›Paper›PMID 38997271›Full record

ArticleCell death & disease2024

Increased ONECUT2 induced by Helicobacter pylori promotes gastric cancer cell stemness via an AKT-related pathway.

Mi Lin, Ru-Hong Tu, Sheng-Ze Wu, Qing Zhong, Kai Weng, Yu-Kai Wu, Guang-Tan Lin, Jia-Bin Wang, Chao-Hui Zheng, Jian-Wei Xie and 5 more

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Article
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  5. Review
  6. Review
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  10. Silencing PPP2R1A inhibits the progression of gastric cancer cells.Journal of cancer research and clinical oncology · 2025
    Article
  11. Review
  12. Article
  13. Article
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

15 authors.

Mi Lin *Department of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Ru-Hong Tu *Department of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.ORCID 0000-0002-7491-3879
Sheng-Ze Wu *Department of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Qing Zhong *Department of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Kai WengDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Yu-Kai WuDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Guang-Tan LinDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Jia-Bin WangDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Chao-Hui ZhengDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Jian-Wei XieDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Jian-Xian LinDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Qi-Yue ChenDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Chang-Ming HuangDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China. hcmlr2002@163.com.ORCID 0000-0002-0019-885X
Long-Long CaoDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China. 1291821982@qq.com.ORCID 0000-0003-3144-3050
Ping LiDepartment of Gastric Surgery, Fujian Medical University Union Hospital, Fuzhou, China. pingli811002@163.com.ORCID 0000-0003-0332-867X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Helicobacter pylori (HP) infection initiates and promotes gastric carcinogenesis. ONECUT2 shows promise for tumor diagnosis, prognosis, and treatment. This study explored ONECUT2's role and the specific mechanism underlying HP infection-associated gastric carcinogenesis to suggest a basis for targeting ONECUT2 as a therapeutic strategy for gastric cancer (GC). Multidimensional data supported an association between ONECUT2, HP infection, and GC pathogenesis. HP infection upregulated ONECUT2 transcriptional activity via NFκB. In vitro and in vivo experiments demonstrated that ONECUT2 increased the stemness of GC cells. ONECUT2 was also shown to inhibit PPP2R4 transcription, resulting in reduced PP2A activity, which in turn increased AKT/β-catenin phosphorylation. AKT/β-catenin phosphorylation facilitates β-catenin translocation to the nucleus, initiating transcription of downstream stemness-associated genes in GC cells. HP infection upregulated the reduction of AKT and β-catenin phosphorylation triggered by ONECUT2 downregulation via ONECUT2 induction. Clinical survival analysis indicated that high ONECUT2 expression may indicate poor prognosis in GC. This study highlights a critical role played by ONECUT2 in promoting HP infection-associated GC by enhancing cell stemness through the PPP2R4/AKT/β-catenin signaling pathway. These findings suggest promising therapeutic strategies and potential targets for GC treatment.

Indexed as

Helicobacter InfectionsHelicobacter pyloriNeoplastic Stem CellsProto-Oncogene Proteins c-aktStomach NeoplasmsAnimalsbeta CateninCell Line, TumorFemaleGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansMaleMiceMice, Inbred BALB CMice, Nudebeta CateninHomeodomain ProteinsONECUT2 protein, humanProtein Phosphatase 2Proto-Oncogene Proteins c-aktTranscription Factors

Identifiers

PMID38997271
PMCPMC11245518

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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.