Evidence map›Paper›PMID 40520011›Full record

ArticleInternational journal of biological sciences2025

Luteolin improves precancerous conditions of the gastric mucosa by binding STAT3 and inhibiting LCN2 expression.

Xinyu Hao, Shouli Yuan, Jing Ning, Yuanfei Zhou, Yanfei Lang, Xiurui Han, Qiao Meng, Ying Xiong, Rongli Cui, Yueqing Gong and 8 more

Abstract read
In one paragraph

Article in International journal of biological sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Recent advances in spasmolytic polypeptide expressing metaplasia research.World journal of gastrointestinal oncology · 2026
    Review
  5. Review
  6. 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

18 authors.

Xinyu HaoDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Shouli YuanPeking-Tsinghua Center for Life Sciences, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China.
Jing NingDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Yuanfei ZhouSynthetic and Functional Biomolecules Center, Beijing National Laboratory for Molecular Sciences, Key Laboratory of Bioorganic Chemistry and Molecular Engineering of Ministry of Education, College of Chemistry and Molecular Engineering, Peking University, Beijing, China.
Yanfei LangDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Xiurui HanDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Qiao MengDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Ying XiongDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Rongli CuiDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Yueqing GongDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Chao MaDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Weichao XuDepartment of Gastroenterology, Hebei Hospital of Traditional Chinese Medicine, Shijiazhuang, China.
Yangang WangDepartment of Gastroenterology, Beijing University of Chinese Medicine Third Affiliated Hospital, Beijing, China.
Xiaohuan GuoInstitute for Immunology, Tsinghua University, Beijing, China.
Chu WangPeking-Tsinghua Center for Life Sciences, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, China.
Jing ZhangDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Weiwei FuDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Shigang DingDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibition of malignant transformation from the precancerous stage has important clinical value for the prevention of gastric cancer. Here, we report a strategy to inhibit precancerous gastric conditions by Luteolin (Lut). Lut treatment resulted in remarkable resistance to oxyntic atrophy, spasmolytic polypeptide-expressing metaplasia (SPEM), and gastric mucosal injury in tamoxifen (TAM)-treated mice, chenodeoxycholic acid-treated rats, and human organoids. Mechanism study suggested that LCN2 expression was upregulated in the SPEM mucosa and downregulated after Lut treatment. LCN2 blocking suppressed TAM-induced oxyntic atrophy and metaplasia and partially counteracted the effect of Lut. Quantitative chemoproteomics identified that Lut bound to STAT3 and inhibited its phosphorylation. Functional experiments using STAT3 inhibitors and epithelial cell-specific

Indexed as

Gastric MucosaLipocalin-2LuteolinPrecancerous ConditionsSTAT3 Transcription FactorAnimalsHumansMaleMiceMice, Inbred C57BLRatsRats, Sprague-DawleyStomach NeoplasmsLipocalin-2LuteolinSTAT3 Transcription FactorGastric cancerLCN2LuteolinPrecancerous gastric conditionsSpasmolytic polypeptide-expressing metaplasiaSTAT3

Identifiers

PMID40520011
PMCPMC12160510

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.