Evidence map›Paper›PMID 31423013›Full record

ArticleCell death & disease2019

SIRT1-targeted miR-543 autophagy inhibition and epithelial-mesenchymal transition promotion in Helicobacter pylori CagA-associated gastric cancer.

Yanyan Shi, Ziwei Yang, Ting Zhang, Lijuan Shen, Yuan Li, Shigang Ding

Open access · goldAbstract 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 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. RSC advances · 2025
    Review
  8. Article
  9. The role of SIRT1 in the development of gastrointestinal tumors.Frontiers in cell and developmental biology · 2025
    Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. [Preparation ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    Article
  15. Article
  16. Review
  17. Review
  18. Programmed cell death inFrontiers in cellular and infection microbiology · 2024
    Review
  19. Review
  20. 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

6 authors at 3 institutions in 1 country.

Yanyan ShiResearch Center of Clinical Epidemiology, Peking University Third Hospital, 100191, Beijing, PR China.
Ziwei YangDepartment of Clinical Laboratory Medicine, The First Affiliated Hospital of China Medical University, Shenyang, 110001, Liaoning, PR China.
Ting ZhangDepartment of Microbiology, Peking University Health Science Center, 100191, Beijing, PR China.
Lijuan ShenDepartment of Gastroenterology, Affiliated Hospital of Qinghai University, 810001, Xining, PR China.
Yuan LiDepartment of Gastroenterology, Peking University Third Hospital, 100191, Beijing, PR China. leeeyuan@aliyun.com.
Shigang DingDepartment of Gastroenterology, Peking University Third Hospital, 100191, Beijing, PR China. dingshigang222@163.com.ORCID http://orcid.org/0000-0002-0831-0965
Peking University · CNFirst Hospital of China Medical University · CNQinghai University Affiliated Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer is an important cause of death worldwide with Helicobacter pylori (H. pylori) considered a leading and known risk factor for its development. More particularly and despite the underlying mechanisms not being very clear, studies have revealed that the H. pylori cytotoxin-associated gene A (CagA) protein plays a key role in this process. In this study it was found that H. pylori increased the expression of miR-543 in human gastric cancer tissue when compared with H. pylori-negative gastric cancer tissue samples. In vitro experiments showed that increased expression of miR-543 induced by CagA is a strong promoter of cell proliferation, migration, and invasion. Conversely, a miR-543 inhibitor suppressed or reversed these effects. It was furthermore found that silencing miR-543 inhibited autophagy and led to epithelial-mesenchymal transition (EMT) under in vitro. The mechanisms by which miR-543 targets SIRT1 to downregulate autophagy was also described. The results suggest that in the progression of H. pylori-associated gastric cancer, CagA induces overexpression of miR-543, which subsequently targets SIRT1 to suppress autophagy. This may be followed by increased expression of EMT causing cell migration and invasion. Consequently, miR-543 might be considered a therapeutic target for H. pylori-associated gastric cancer.

Indexed as

Antigens, BacterialAutophagyBacterial ProteinsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHelicobacter InfectionsHelicobacter pyloriHumansMicroRNAsNeoplasm InvasivenessSirtuin 1Stomach NeoplasmsTransfectionAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriMicroRNAsMIRN543 microRNA, humanSIRT1 protein, humanSirtuin 1

Identifiers

PMID31423013
PMCPMC6698481
OpenAlexW2968303353

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.