Evidence map›Paper›PMID 33111209›Full record

ArticleGastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association2021

Tumor suppressor ATP4B serve as a promising biomarker for worsening of gastric atrophy and poor differentiation.

Yuanming Pan, Xin Wang, Yuqi He, Shuye Lin, Min Zhu, Yangjie Li, Jianxun Wang, Jiheng Wang, Xianzong Ma, Junfeng Xu and 5 more

Abstract read
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In one paragraph

Article in Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association, 2021. 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
0.6field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  7. Autoimmune Gastritis andInternational journal of molecular sciences · 2025
    Review
  8. ComprehensiveOncology reports · 2025
    Review
  9. Article
  10. Identification of gastric cancer biomarkers throughBiochemistry and biophysics reports · 2024
    Article
  11. Review
  12. Review
  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 at 4 institutions in 3 countries.

Yuanming Pan *Department of Gastroenterology, the 7th Medical Center of Chinese PLA General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, China.
Xin Wang *Department of Gastroenterology, the 7th Medical Center of Chinese PLA General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, China.
Yuqi He *Department of Gastroenterology, the 7th Medical Center of Chinese PLA General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, China.
Shuye LinLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital/Institute, No. 52 Fucheng Road, Haidian District, Beijing, 100142, China.
Min ZhuLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital/Institute, No. 52 Fucheng Road, Haidian District, Beijing, 100142, China.
Yangjie LiDepartment of Gastroenterology, the 7th Medical Center of Chinese PLA General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, China.
Jianxun WangSchool of Basic Medical Sciences, Qingdao University, Qingdao, China.
Jiheng WangDepartment of Gastroenterology, the 7th Medical Center of Chinese PLA General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, China.
Xianzong MaDepartment of Gastroenterology, the 7th Medical Center of Chinese PLA General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, China.
Junfeng XuDepartment of Gastroenterology, the 7th Medical Center of Chinese PLA General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, China.
Lang YangDepartment of Gastroenterology, the 7th Medical Center of Chinese PLA General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, China.
Guibin YangDepartment of Gastroenterology, Aerospace Clinic Medical College of Peking University, No. 15 Yuanquan Road, Haidian District, Beijing, 100049, China.
Jiaqiang HuangCollege of Life Sciences and Bioengineering, School of Science, Beijing Jiaotong University, 3 Shangyuan Residence, Haidian District, Beijing, 100044, China. jqhuang@bjtu.edu.cn.
Youyong LuLaboratory of Molecular Oncology, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital/Institute, No. 52 Fucheng Road, Haidian District, Beijing, 100142, China. youyonglu@hsc.pku.edu.cn.
Jianqiu ShengDepartment of Gastroenterology, the 7th Medical Center of Chinese PLA General Hospital, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, China. jianqiu@263.net.ORCID http://orcid.org/0000-0001-8930-2117
Chinese PLA General Hospital · CNPeking University · CNQingdao University · CNBeijing Jiaotong University · CN

Funding

China Postdoctoral Science Foundation No.2017M613421Natural Science Foundation of Beijing Municipality No.7172213Project of Army Special Care No.12BJZ04
6 · The paper itself

Abstract

backgroundHydrogen/potassium ATPase β (ATP4B) is a proton pump acting an essential role in gastric acid secretion. This study aimed to investigate the diagnostic performance of ATP4B and its biological role in tumor progression in gastric cancer.

methodsThe correlations between ATP4B expression level and clinicopathologic parameters, as well as the relevance of ATP4B expression with overall survival were assessed. The functional roles of ATP4B in gastric cancer were verified by gain- and loss-of-function cell models and tumor xenograft models. The possible downstream effects of ATP4B were analyzed by iTRAQ-based quantitative proteomics analysis.

resultsA dramatic decrease in ATP4B was associated with malignant transformation in gastric mucosa lesions and correlated with poor differentiation. Restoration of ATP4B expression in gastric cancer cells significantly suppressed cell proliferation, cell viability, migration, invasion, tumorigenicity and induced apoptosis, whereas ATP4B silencing exerted the opposite effects. Mechanistically, we found a quality control on mitochondrial metabolism and functions in ATP4B-overexpression GC cells.

conclusionsOur data suggest that decreasing ATP4B is an indicator for gastric mucosa malignant transformation and GC aggressive phenotype and it plays an inhibitory role in gastric cancer as a tumor suppressor via regulating mitochondrial metabolism and apoptosis pathway.

Indexed as

AtrophyBiomarkers, TumorCarcinogenesisCell DifferentiationCell Line, TumorCell Transformation, NeoplasticFemaleGastric MucosaGastritis, AtrophicGenes, Tumor SuppressorHumansMaleMiddle AgedPhenotypePlasma Membrane Calcium-Transporting ATPasesPrognosisATP2B4 protein, humanBiomarkers, TumorPlasma Membrane Calcium-Transporting ATPasesATP4BGastric cancerMalignant transformationMitochondrion

Identifiers

PMID33111209
OpenAlexW3097960398

What OpenQuestion holds

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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.