Evidence map›Paper›PMID 40181153›Full record

ArticleOncogene2025

Suprabasin promotes gastric cancer liver metastasis via hepatic stellate cells-mediated EGF/CCL2/JAK2 intercellular signaling pathways.

Difeng Li, Zhiqing Gao, Zhuojun Zhang, Han Chen, Ruiming Tang, Lihuan Zhou, Yingmin Ye, Jiaqian Lin, Ping Zhou, Chanjuan Wang and 12 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 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. Inflammatory factors collaboratively linkFrontiers in immunology · 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

22 authors.

Difeng Li *The Affiliated Qingyuan Hospital (Qingyuan People's Hospital), Guangzhou Medical University, Qingyuan, China.
Zhiqing Gao *Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, Guangzhou Medical University, Guangzhou, China.
Zhuojun Zhang *Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, Guangzhou Medical University, Guangzhou, China.
Han Chen *Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, Guangzhou Medical University, Guangzhou, China.
Ruiming Tang *The Affiliated Qingyuan Hospital (Qingyuan People's Hospital), Guangzhou Medical University, Qingyuan, China.
Lihuan Zhou *The Affiliated Qingyuan Hospital (Qingyuan People's Hospital), Guangzhou Medical University, Qingyuan, China.
Yingmin YeDepartment of Pathogen Biology and Immunology, School of Basic Courses, Guangdong Pharmaceutical University, Guangzhou, China.
Jiaqian LinGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, Guangzhou Medical University, Guangzhou, China.
Ping ZhouGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, Guangzhou Medical University, Guangzhou, China.
Chanjuan WangGuangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, Guangzhou Medical University, Guangzhou, China.
Xiaoli FengThe Affiliated Qingyuan Hospital (Qingyuan People's Hospital), Guangzhou Medical University, Qingyuan, China.
Yaoming HeDepartment of Gastrointestinal Surgery, Jiangmen Central Hospital, Jiangmen, China.
Zijie MengClinical Experimental Center, Jiangmen Engineering Technology Research Center of Clinical Biobank and Translational Research, Jiangmen Central Hospital, Jiangmen, China.
Mingzhu ZhengClinical Experimental Center, Jiangmen Engineering Technology Research Center of Clinical Biobank and Translational Research, Jiangmen Central Hospital, Jiangmen, China.
Wenjie LuClinical Experimental Center, Jiangmen Engineering Technology Research Center of Clinical Biobank and Translational Research, Jiangmen Central Hospital, Jiangmen, China.
Zhengfu FengThe Affiliated Qingyuan Hospital (Qingyuan People's Hospital), Guangzhou Medical University, Qingyuan, China.
Lan WangDepartment of Pathogen Biology and Immunology, School of Basic Courses, Guangdong Pharmaceutical University, Guangzhou, China.
Yuanyuan PeiDepartment of Central Laboratory, Longgang District Maternity & Child Healthcare Hospital of Shenzhen City (Longgang Maternity and Child Institute of Shantou University Medical College), Shenzhen, China.
Jianan YangDepartment of Urologic Oncosurgery, Guangzhou Institute of Cancer Research, The Affiliated Cancer Hospital, Guangzhou Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0002-1369-836X
Tianyu TaoCancer Institute, Southern Medical University, Guangzhou, China.
Xin ZhangClinical Experimental Center, Jiangmen Engineering Technology Research Center of Clinical Biobank and Translational Research, Jiangmen Central Hospital, Jiangmen, China. zhangx45@mail3.sysu.edu.cn.
Lili JiangThe Affiliated Qingyuan Hospital (Qingyuan People's Hospital), Guangzhou Medical University, Qingyuan, China. jianglili@gzhmu.edu.cn.ORCID http://orcid.org/0000-0003-2361-5975

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer is among the most prevalent gastrointestinal tumors, with liver metastasis significantly worsening patient outcomes. While hepatic stellate cell activation is crucial in hepatocellular carcinoma progression and liver metastasis, its role in gastric cancer liver metastasis is not well understood. In this study, we identified Suprabasin (SBSN) as a key oncogene driving gastric cancer liver metastasis. SBSN was upregulated in gastric cancer tissues and further elevated in liver metastasis, correlating with poor prognosis. Mechanistically, SBSN promoted proliferation, migration, and invasion of gastric cancer cells by activating the STAT3 signaling pathway, as shown in vitro and in vivo. Using a co-culture model of gastric cancer cells and hepatic stellate cell line LX-2, we found that increased SBSN expression in gastric cancer cells triggered EGF secretion, activating LX-2 cells through the EGF/EGFR axis. Activated LX-2 cells then secreted CCL2, initiating the CCL2/CCR2/JAK2 signaling pathway in gastric cancer cells, facilitating their migration to the liver and promoting colonization and growth. Our findings highlight the prognostic significance of SBSN in gastric cancer and liver metastasis, suggesting it as a potential biomarker for disease progression. The SBSN-mediated EGF/EGFR and CCL2/CCR2/JAK2 signaling axes are critical for LX-2 activation and gastric cancer cell migration, offering a rationale for targeting SBSN in treating gastric cancer liver metastasis.

Indexed as

Chemokine CCL2Epidermal Growth FactorHepatic Stellate CellsJanus Kinase 2Liver NeoplasmsStomach NeoplasmsAnimalsCell Line, TumorCell MovementCell ProliferationErbB ReceptorsFemaleGene Expression Regulation, NeoplasticHumansMaleMiceCCL2 protein, humanChemokine CCL2EGFR protein, humanEpidermal Growth FactorErbB ReceptorsJAK2 protein, humanJanus Kinase 2

Identifiers

PMID40181153

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.