Evidence map›Paper›PMID 41306771›Full record

ArticleResearch (Washington, D.C.)2025

ATPase Inhibitory Factor 1 Drives Mitochondrial Energy Metabolic Reprogramming to Promote HCC Vasculogenic Mimicry via the ESR1/miR-20a-3p/GNAZ Pathway.

Shilun Wu, Changyu Yao, Lu Fang, Yiwen Sun, Mingming Zhao, Jie Chen, Gaofei Hu, Zhe Zhao, Shusi Ding, Jing Xue and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Research (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

14 authors.

Shilun WuDepartment of Hepatobiliary Surgery, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Changyu YaoDepartment of Hepatobiliary Surgery, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Lu FangThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China.
Yiwen SunDepartment of Pathology, Peking University People's Hospital, Peking University, Beijing 100044, China.
Mingming ZhaoDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, Beijing, China.
Jie ChenThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China.
Gaofei HuThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China.
Zhe ZhaoDepartment of Pharmacy, Peking University Third Hospital; Institute for Drug Evaluation, Peking University Health Science Center, Beijing 100191, China.
Shusi DingBeijing Tiantan Hospital, China National Clinical Research Center for Neurological Diseases, Advanced Innovation Center for Human Brain Protection, Beijing Institute of Brain Disorders, The Capital Medical University, Beijing 100050, China.
Jing XueBeijing Tiantan Hospital, China National Clinical Research Center for Neurological Diseases, Advanced Innovation Center for Human Brain Protection, Beijing Institute of Brain Disorders, The Capital Medical University, Beijing 100050, China.
Xiaoyi LiuThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China.
Wenbing SunDepartment of Hepatobiliary Surgery, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Jian KongDepartment of Hepatobiliary Surgery, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Lemin ZhengThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China.ORCID https://orcid.org/0000-0003-4473-6936

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vasculogenic mimicry (VM) is a microcirculation pattern that has a crucial effect on hepatocellular carcinoma (HCC) metastasis. In this study, leveraging the GeneCard and The Cancer Genome Atlas databases, we identified ATPase inhibitory factor 1 (IF1) as a potential regulator of VM formation. Our research findings indicate that IF1 can promote HCC cell tube formation in vitro and enhance HCC VM and lung metastasis in vivo. Transcriptome sequencing combined with in vivo experiments revealed that IF1 knockdown elevates miR-20a-3p expression. Lentivirus-mediated miR-20a-3p overexpression reversed IF1-induced VM. Dual-luciferase reporter gene assays showed that estrogen receptor 1 (ESR1) acts as a transcription factor of the miR-20a-3p precursor. Further mechanistic studies revealed that excessive reactive oxygen species accumulation caused by IF1-induced mitochondrial metabolic reprogramming can inhibit ESR1 expression by promoting DNA methylation of its promoter. G protein subunit alpha Z (GNAZ), a miR-20a-3p target protein, can promote VM by phosphorylating components of the ERK pathway. Collectively, these results delineate a novel IF1/ESR1/miR-20a-3p/GNAZ axis in HCC VM and metastasis, providing potential therapeutic targets.

Identifiers

PMID41306771
PMCPMC12645449

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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.