Evidence map›Paper›PMID 30778796›Full record

ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2019

Epigenetic downregulation of MUC17 by H. pylori infection facilitates NF-κB-mediated expression of CEACAM1-3S in human gastric cancer.

Shuye Lin, Yaping Zhang, Yingqi Hu, Bing Yang, Jiantao Cui, Jiaqiang Huang, Ji Ming Wang, Rui Xing, Youyong Lu

Open access · bronzeAbstract read
In one paragraph

Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. CAR-T cell therapy targeting MUC17 in gastric tumors.Journal for immunotherapy of cancer · 2025
    Article
  7. The intersection ofFrontiers in cellular and infection microbiology · 2025
    Review
  8. Review
  9. Epigenetic alterations inJournal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2025
    Review
  10. Review
  11. Article
  12. DifferentialOncology reports · 2021
    Observational
  13. Review
  14. Article
  15. Systematic profiling of alternative splicing inCancer cell international · 2020
    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

9 authors at 3 institutions in 3 countries.

Shuye LinLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, 100142, People's Republic of China.
Yaping ZhangLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, 100142, People's Republic of China.
Yingqi HuLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, 100142, People's Republic of China.
Bing YangLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, 100142, People's Republic of China.
Jiantao CuiLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, 100142, People's Republic of China.
Jiaqiang HuangCollege of Life Sciences and Bioengineering, School of Science, Beijing Jiaotong University, 3 Shangyuancun, Haidian District, Beijing, 100044, People's Republic of China.
Ji Ming WangCancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD, 21702, USA.
Rui XingLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, 100142, People's Republic of China. xingrui@bjmu.edu.cn.
Youyong LuLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, Beijing, 100142, People's Republic of China. youyonglu@bjmu.edu.cn.ORCID http://orcid.org/0000-0003-4877-1093
Peking University · CNBeijing Jiaotong University · CNNational Cancer Institute · US

Funding

The Role of Cellular Receptors Involved in Inflammation and Tumor ProgressionZIABC010015 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, JI MING · 2009 to 2023
$6.3M
Intramural NIH HHS ZIA BC010015National Natural Science Foundation of China 81872021Natural Science Foundation of Beijing Municipality 7182027
6 · The paper itself

Abstract

BACKGROUND AND

aimsHelicobacter pylori invades the mucosal barrier and infects the mucins of gastric epithelial cells. However, whether gastric carcinogenesis caused by H. pylori infection involves the membrane-bound mucins is unclear. This study explored the role of mucin 17 (MUC17) in gastric cancer (GC) associated with H. pylori infection.

methodsThe expression of MUC17 and carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) was examined in human GC cells and tissues with H. pylori infection. Gain- and loss-of-function assays were performed to assess the role of MUC17 in regulating CEACAM1 in H. pylori-infected GC cells.

resultsMUC17 was downregulated in H. pylori-infected GC cells and tissues in association with poor survival of GC patients. Downregulation of MUC17 was attributable to MUC17 promoter methylation mediated by DNA methyltransferase 1 (DNMT1) H. pylori-enhanced GC cell proliferation and colony formation associated with MUC17 downregulation. Gain- and loss-of-function assays showed that MUC17 inhibited the H. pylori-enhanced GC cell growth by preventing the translocation of H. pylori CagA into GC cells. Moreover, MUC17 downregulated the expression of CEACAM1 variant 3S (CEACAM1-3S) in GC cells and tissues with H. pylori infection. Additionally, MUC17 downregulated CEACAM1 promoter activity via attenuation of NF-κB activation in GC cells.

conclusionsMUC17 was epigenetically downregulated in GC with H. pylori infection. MUC17 inhibited H. pylori CagA translocation via attenuation of NF-κB-mediated expression of CEACAM1-3S in GC cells. Thus, MUC17 may serve as a valuable prognostic biomarker for H. pylori-associated GC.

Indexed as

Epigenesis, GeneticGene Expression Regulation, NeoplasticAntigens, CDApoptosisBiomarkers, TumorCell Adhesion MoleculesCell ProliferationFemaleFollow-Up StudiesHelicobacter InfectionsHelicobacter pyloriHumansMaleMiddle AgedMucinsNF-kappa BAntigens, CDBiomarkers, TumorCD66 antigensCell Adhesion MoleculesMUC17 protein, humanMucinsNF-kappa BCagACEACAM1Gastric cancerH. pyloriMucin 17

Identifiers

PMID30778796
PMCPMC8320707
OpenAlexW2914071842

What OpenQuestion holds

Textmetadata
LicenceTDM
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.