Evidence map›Paper›PMID 41203799›Full record

ArticleScientific reports2025

Metabolic syndrome-related gene signature for prognosis and immune microenvironment prediction in hepatocellular carcinoma.

Liuyan Chen, Yaobin Wang, Shuai Li, Shan Lu, Yiling Luo, Yanping Ning, Jifei Chen, Sufang Zhou

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

8 authors.

Liuyan Chen *State Key Laboratory of Targeting Oncology, National Center for International Research of Bio-targeting Theranostics, Guangxi Key Laboratory of Bio-targeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Talent Highland of Major New Drugs Innovation and Development, Targeting Theranostics Research Center of Guangxi Higher Education, Guangxi Medical University, Nanning, 530021, Guangxi, China.
Yaobin Wang *Key Laboratory of Biological Molecular Medicine Research, Guangxi Medical University, Education Department of Guangxi Zhuang Autonomous Region, Nanning, 530021, Guangxi, China.
Shuai Li *Key Laboratory of Biological Molecular Medicine Research, Guangxi Medical University, Education Department of Guangxi Zhuang Autonomous Region, Nanning, 530021, Guangxi, China.
Shan LuDepartment of Obstetrics and Gynecology, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, 545007, Guangxi, China.
Yiling LuoKey Laboratory of Biological Molecular Medicine Research, Guangxi Medical University, Education Department of Guangxi Zhuang Autonomous Region, Nanning, 530021, Guangxi, China.
Yanping NingDepartment of lmmunology, School of Basic Medical Sciences, Guangxi Medical University, Nanning, 530021, China.
Jifei ChenAcute Respiratory Infectious Diseases Network Laboratory, Department of Science and Education, GCP Institutional Office, Biobank of Guangxi Chest Hospital, Liuzhou, 545005, Guangxi, China. chen880108@hotmail.com.
Sufang ZhouState Key Laboratory of Targeting Oncology, National Center for International Research of Bio-targeting Theranostics, Guangxi Key Laboratory of Bio-targeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Talent Highland of Major New Drugs Innovation and Development, Targeting Theranostics Research Center of Guangxi Higher Education, Guangxi Medical University, Nanning, 530021, Guangxi, China. 437574096@qq.com.

Funding

National Natural Science Foundation of China 82060470National Natural Science Foundation of China 82273103
6 · The paper itself

Abstract

Metabolic syndrome is a major risk factor for hepatocellular carcinoma (HCC) progression, yet the role of metabolic syndrome-related genes in HCC remains incompletely understood. Using bioinformatics approaches, we investigated the influence of these genes on HCC prognosis and tumor biology. Two distinct patient clusters (C1 and C2) were identified based on metabolic gene expression, with C2 exhibiting poorer survival, increased stemness, and higher risk scores. A risk model further revealed that high-risk patients had worse outcomes, elevated immunosuppressive cell infiltration, and distinct phenotypic features. Experimental validation via qRT-PCR confirmed upregulation of risk model genes (particularly KIAA1841 and TUBA1B) in HCC cell lines and patient blood samples. Notably, post-surgical declines in KIAA1841 and TUBA1B levels were observed. Our findings highlight the clinical relevance of metabolic syndrome-related genes in HCC, linking them to prognosis, tumor microenvironment remodeling, cancer stemness, and immunotherapy response.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsMetabolic SyndromeTumor MicroenvironmentCell Line, TumorFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMiddle AgedPrognosisTranscriptomeHepatocellular carcinomaImmunotherapyMetabolic syndromeStemness indexTumor microenvironment

Identifiers

PMID41203799
PMCPMC12594785

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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.