Evidence map›Paper›PMID 38849840›Full record

ArticleMolecular cancer2024

OLFM4 promotes the progression of intestinal metaplasia through activation of the MYH9/GSK3β/β-catenin pathway.

Hongfa Wei, Wenchao Li, Leli Zeng, Ni Ding, Kuan Li, Hong Yu, Fei Jiang, Haofan Yin, Yu Xia, Cuncan Deng and 8 more

Abstract read
In one paragraph

Article in Molecular cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

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  10. Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 2026
    Review
  11. Review
  12. FUT2-Mediated Fucosylation of OLFM4 Promotes Colon Cancer Cell Differentiation.Canadian journal of gastroenterology & hepatology · 2026
    Article
  13. Review
  14. Olfactomedin 4 in cancer development and progression.Biochimica et biophysica acta. Reviews on cancer · 2025
    Review
  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Hongfa WeiDepartment of General Surgery, The First Affiliated Hospital of Shantou University Medical College, Jinping, Shantou, Guangdong, 515041, P.R. China.
Wenchao LiDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Leli ZengScientific Research Center, The Biobank, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, 518107, Guangdong, P.R. China.
Ni DingScientific Research Center, The Biobank, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, 518107, Guangdong, P.R. China.
Kuan LiDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Hong YuDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Fei JiangDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Haofan YinDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Yu XiaScientific Research Center, The Biobank, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, 518107, Guangdong, P.R. China.
Cuncan DengDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Nan CaiDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Xiancong ChenDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Liang GuDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China.
Huanjie ChenDepartment of General Surgery, The First Affiliated Hospital of Shantou University Medical College, Jinping, Shantou, Guangdong, 515041, P.R. China.
Feiran ZhangDepartment of General Surgery, The First Affiliated Hospital of Shantou University Medical College, Jinping, Shantou, Guangdong, 515041, P.R. China. feiran.z@126.com.
Yulong HeDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China. heyulong@mail.sysu.edu.cn.
Jia LiDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China. lijia88@mail.sysu.edu.cn.
Changhua ZhangDepartment of Gastrointestinal Surgery, Digestive Diseases Center, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen, 518107, China. zhangchanghua@sysush.com.

Funding

Guangdong Basic and Applied Basic Research Foundation 2023A1515010156Guangdong Provincial Key Laboratory of Digestive Cancer Research 2021B1212040006He Yulong Expert Workstation of Yunnan Province 202104AC100001-B03Science and Technology Special Project of the National Sustainable Development Agenda Innovation Demonstration Zone of Yunnan Province 202104 AC100001-A10the National Natural Science Foundation of China 22307151the Science and Technology Planning Project of Shenzhen Municipality GJHZ20220913142400001the Science and Technology Planning Project of Shenzhen Municipality JCYJ20220530144815035
6 · The paper itself

Abstract

backgroundIntestinal metaplasia (IM) is classified into complete intestinal metaplasia (CIM) and incomplete intestinal metaplasia (IIM). Patients diagnosed with IIM face an elevated susceptibility to the development of gastric cancer, underscoring the critical need for early screening measures. In addition to the complexities associated with diagnosis, the exact mechanisms driving the progression of gastric cancer in IIM patients remain poorly understood. OLFM4 is overexpressed in several types of tumors, including colorectal, gastric, pancreatic, and ovarian cancers, and its expression has been associated with tumor progression.

methodsIn this study, we used pathological sections from two clinical centers, biopsies of IM tissues, precancerous lesions of gastric cancer (PLGC) cell models, animal models, and organoids to explore the role of OLFM4 in IIM.

resultsOur results show that OLFM4 expression is highly increased in IIM, with superior diagnostic accuracy of IIM when compared to CDX2 and MUC2. OLFM4, along with MYH9, was overexpressed in IM organoids and PLGC animal models. Furthermore, OLFM4, in combination with Myosin heavy chain 9 (MYH9), accelerated the ubiquitination of GSK3β and resulted in increased β-catenin levels through the Wnt signaling pathway, promoting the proliferation and invasion abilities of PLGC cells.

conclusionsOLFM4 represents a novel biomarker for IIM and could be utilized as an important auxiliary means to delimit the key population for early gastric cancer screening. Finally, our study identifies cell signaling pathways involved in the progression of IM.

Indexed as

beta CateninDisease ProgressionGlycogen Synthase Kinase 3 betaMetaplasiaMyosin Heavy ChainsAnimalsCell Line, TumorCell ProliferationDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticHumansMaleMiceOrganoidsStomach Neoplasmsbeta CateninGlycogen Synthase Kinase 3 betaMYH9 protein, humanMyosin Heavy Chains

Identifiers

PMID38849840
PMCPMC11157765

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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.