Evidence map›Paper›PMID 40185720›Full record

ReviewCell death discovery2025

Roles of the gut microbiota in hepatocellular carcinoma: from the gut dysbiosis to the intratumoral microbiota.

Yiqin Wang, Yongqiang Li, Yong Lin, Chuangyu Cao, Dongcheng Chen, Xianguang Huang, Canhua Li, Haoming Xu, Huasheng Lai, Huiting Chen and 1 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
–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

37 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

11 authors.

Yiqin Wang *Department of Gastroenterology and Hepatology, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, China.ORCID http://orcid.org/0000-0003-1575-1571
Yongqiang Li *Department of Gastroenterology and Hepatology, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Yong Lin *Department of Gastroenterology and Hepatology, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Chuangyu CaoDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Dongcheng ChenDepartment of Gastroenterology and Hepatology, Baiyun Hospital of Guangzhou First People's Hospital (The Second People's Hospital of Baiyun District), Guangzhou, China.
Xianguang HuangDepartment of Gastroenterology and Hepatology, Baiyun Hospital of Guangzhou First People's Hospital (The Second People's Hospital of Baiyun District), Guangzhou, China.
Canhua LiDepartment of Gastroenterology and Hepatology, Baiyun Hospital of Guangzhou First People's Hospital (The Second People's Hospital of Baiyun District), Guangzhou, China.
Haoming XuDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Huasheng LaiDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Huiting ChenDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, China. eychenhuiting@scut.edu.cn.ORCID http://orcid.org/0000-0003-0380-7822
Yongjian ZhouDepartment of Gastroenterology and Hepatology, The Second Affiliated Hospital, School of Medicine, South China University of Technology, Guangzhou, China. eyzhouyongjian@scut.edu.cn.ORCID http://orcid.org/0000-0003-1721-7639

Funding

National Science Foundation of China | Young Scientists Fund No. NSFC 82100124
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is closely linked to alterations in the gut microbiota. This dysbiosis is characterized by significant changes in the microbial population, which correlate with the progression of HCC. Gut dysbiosis ultimately promotes HCC development in several ways: it damages the integrity of the gut-vascular barrier (GVB), alters the tumor microenvironment (TME), and even affects the intratumoral microbiota. Subsequently, intratumoral microbiota present a characteristic profile and play an essential role in HCC progression mainly by causing DNA damage, mediating tumor-related signaling pathways, altering the TME, promoting HCC metastasis, or through other mechanisms. Both gut microbiota and intratumoral microbiota have dual effects on HCC progression; a comprehensive understanding of their complex biological roles will provide a theoretical foundation for potential clinical applications in HCC treatment.

Identifiers

PMID40185720
PMCPMC11971373

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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.