Evidence map›Paper›PMID 40056162›Full record

ArticleCarcinogenesis2025

Olfactomedin 4 promotes gastric cancer cell G2/M progression and serves as a therapeutic target in gastric adenocarcinoma.

Wenli Liu, Hongzhen Li, Istvan Botos, Chutima Kumkhaek, Jianqiong Zhu, Griffin P Rodgers

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Carcinogenesis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Olfactomedin 4 in cancer development and progression.Biochimica et biophysica acta. Reviews on cancer · 2025
    Review
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.

Wenli LiuMolecular and Clinical Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bldg. 10, Room 9N119, 9000 Rockville Pike, Bethesda, MD 20892, United States.ORCID 0000-0002-7499-754X
Hongzhen LiMolecular and Clinical Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bldg. 10, Room 9N119, 9000 Rockville Pike, Bethesda, MD 20892, United States.
Istvan BotosLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bldg. 10, Room 9N119, 9000 Rockville Pike, Bethesda, MD 20892, United States.
Chutima KumkhaekMolecular and Clinical Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bldg. 10, Room 9N119, 9000 Rockville Pike, Bethesda, MD 20892, United States.
Jianqiong ZhuMolecular and Clinical Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bldg. 10, Room 9N119, 9000 Rockville Pike, Bethesda, MD 20892, United States.
Griffin P RodgersMolecular and Clinical Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bldg. 10, Room 9N119, 9000 Rockville Pike, Bethesda, MD 20892, United States.

Funding

NHLBI NIH HHSNIH HHS
6 · The paper itself

Abstract

Olfactomedin 4 (OLFM4) is a member of the olfactomedin domain-containing olfactomedin glycoprotein family and plays important roles in innate immunity, inflammation, and cancer. It exhibits increased expression in gastric cancer patient tissues and has been shown to regulate proliferation and apoptosis in gastric cancer cells. However, the molecular mechanism(s) underlying OLFM4's role in gastric cancer remain unknown. In this study, we found that OLFM4 knockdown significantly inhibited YCC3 gastric cancer cell proliferation and induced G2/M cell cycle arrest. Yeast two-hybridization screening revealed that OLFM4 directly interacts with cyclin B1 interacting protein 1 (CCNB1IP1), an E3 ubiquitin protein ligase. In YCC3 cells, OLFM4 co-immunoprecipitated and colocalized with CCNB1IP1 and underwent cell cycle phase-specific nucleo-cytoplasmic shuttling. OLFM4 knockdown decreased both cyclin B1 protein levels and CDK1 activity in YCC3 cells. Screening of a cohort of OLFM4-targeted microRNAs (miRNAs) for their impact on cell proliferation identified several that significantly downregulated OLFM4 protein levels and inhibited YCC3 cell proliferation in vitro. Rescue experiments demonstrated that these miRNAs' inhibitory effect on cell proliferation was partially related to their downregulation of OLFM4. When three of these miRNAs were individually administered intratumorally to nude mice bearing YCC3 cell xenografts, tumor growth was significantly inhibited when compared with tumors treated with a negative control miRNA. These results suggest that OLFM4 promotes cell cycle progression and cell proliferation in gastric cancer cells and may have utility as a therapeutic target in gastric adenocarcinoma.

Indexed as

AdenocarcinomaGranulocyte Colony-Stimulating FactorStomach NeoplasmsAnimalsApoptosisCell Line, TumorCell ProliferationCyclin B1G2 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticHumansMiceMice, NudeMicroRNAsXenograft Model Antitumor AssaysCyclin B1Granulocyte Colony-Stimulating FactorMicroRNAsOLFM4 protein, humanCCNB1IP1gastric cancerOLFM4

Identifiers

PMID40056162
PMCPMC12013284

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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.