Evidence map›Paper›PMID 40290518›Full record

ArticleJHEP reports : innovation in hepatology2025

PLOD1 promotes the malignancy of hepatocellular carcinoma by facilitating the NF-κB/IL-6/STAT3-dependent TCA cycle.

Chengfei Zhang, Yangchun Zhou, Minghua Hu, Yue Pan, Xin Chen, Qi Sun, Zhijie Ma, Cheng Wang, Yong Zha, Feng Zhu and 1 more

Abstract read
In one paragraph

Article in JHEP reports : innovation in hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
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  3. Metabolic-epigenetic reprogrammingActa pharmaceutica Sinica. B · 2026
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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.

Chengfei ZhangDepartment of General Surgery, Sir Run Run Hospital, Nanjing Medical University, Nanjing, China.
Yangchun ZhouDepartment of General Surgery, Sir Run Run Hospital, Nanjing Medical University, Nanjing, China.
Minghua HuDepartment of Surgery, The First Affiliated Hospital of Wannan Medical College (Yijishan Hospital), Wuhu, China.
Yue PanDepartment of General Surgery, Sir Run Run Hospital, Nanjing Medical University, Nanjing, China.
Xin ChenDepartment of General Surgery, Sir Run Run Hospital, Nanjing Medical University, Nanjing, China.
Qi SunDepartment of Pathology, Nanjing Drum Tower Hospital & National Health Commission Key Laboratory of Antibody Techniques & School of Basic Medical Sciences of Nanjing Medical University, Nanjing, China.
Zhijie MaDepartment of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Cheng WangDepartment of Pathology, Nanjing Drum Tower Hospital & National Health Commission Key Laboratory of Antibody Techniques & School of Basic Medical Sciences of Nanjing Medical University, Nanjing, China.
Yong ZhaHepatobiliary Pancreatic Surgery, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, Kunming, China.
Feng ZhuDepartment of General Surgery, Sir Run Run Hospital, Nanjing Medical University, Nanjing, China.
Hongping XiaZhongda Hospital, School of Medicine, Advanced Institute for Life and Health, Southeast University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aims: Procollagen lysyl hydroxylase 1 (PLOD1) is crucial in regulating collagen synthesis and cross-linking. However, its roles and underlying mechanisms in the progression of hepatocellular carcinoma (HCC) remain unclear. Herein, we aimed to investigate the underlying biological functions and mechanisms of PLOD1 in HCC. Methods: The expression levels of PLOD1 in HCC were measured by qPCR, Western blot, and immunohistochemistry. Cell proliferation, apoptosis, and stemness were examined by CCK8, flow cytometry, sphere formation, and aldehyde dehydrogenase activity assays. The subcutaneous tumorigenicity model, orthotopic tumorigenicity model, and hepatotoxin-induced HCC model were used for Results: PLOD1 is found to be highly expressed in both human ( Conclusions: Our study uncovers the PLOD1/NF-κB/IL-6/STAT3 axis as a therapeutic target for inhibiting the progression and stemness of HCC. Impact and implications: The roles and underlying mechanisms of PLOD1 in the progression of HCC remain unclear. In this study, we report that PLOD1 is highly expressed in patients with HCC and promotes the proliferation and stemness of HCC cells by activating the NF-κB/IL-6/STAT3-dependent TCA cycle. Knocking down hepatic PLOD1 using adeno-associated virus results in reduced progression of HCC in mice, suggesting that PLOD1 may serve as a potential therapeutic target for HCC.

Indexed as

HCCNF-κBPLOD1STAT3TCA cycleTumor stem cell

Identifiers

PMID40290518
PMCPMC12023786

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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.