Evidence map›Paper›PMID 39966385›Full record

ArticleNature communications2025

A glucose-enriched lung pre-metastatic niche triggered by matrix stiffness-tuned exosomal miRNAs in hepatocellular carcinoma.

Yingying Zhao, Hongmei Yu, Jiajun Li, Jiali Qian, Miao Li, Xi Zhang, Mimi Wang, Yaohui Wang, Yinying Dong, Yang You and 9 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

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  20. Deciphering organotropism reveals therapeutic targets in metastasis.Frontiers in cell and developmental biology · 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

19 authors.

Yingying Zhao *Liver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.ORCID http://orcid.org/0009-0009-9166-9378
Hongmei Yu *Liver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.
Jiajun Li *Liver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.
Jiali QianDepartment of Endocrinology, Huashan Hospital, Fudan University, Shanghai, PR China.
Miao LiLiver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.ORCID http://orcid.org/0000-0001-7840-7511
Xi ZhangLiver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.ORCID http://orcid.org/0009-0007-2498-9000
Mimi WangLiver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.ORCID http://orcid.org/0000-0002-9727-8943
Yaohui WangDepartment of Interventional Radiology, Fudan University Shanghai Cancer Center, Shanghai, PR China.
Yinying DongDepartment of Radiation Oncology, The Affiliated Hospital of Qingdao University, Qingdao, PR China.
Yang YouDepartment of Oncology, Zhongshan Hospital, Fudan University, Shanghai, PR China.
Qiwen ZhouDepartment of Oncology, Zhongshan Hospital, Fudan University, Shanghai, PR China.ORCID http://orcid.org/0000-0002-6598-5643
Dongmei GaoLiver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.
Yan ZhaoLiver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.
Binbin LiuLiver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.ORCID http://orcid.org/0000-0002-3458-4046
Rongxin ChenLiver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.
Zhenggang RenLiver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China.
Zhiming WangDepartment of Oncology, Zhongshan Hospital, Fudan University, Shanghai, PR China. wang.zhiming@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0002-7605-377X
Kezhi ZhangDepartment of Hepatobiliary Surgery, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou School of Clinical Medicine, Nanjing Medical University, Taizhou, Jiangsu Province, PR China. zkz97@njmu.edu.cn.ORCID http://orcid.org/0009-0005-7775-8500
Jiefeng CuiLiver Cancer Institute, Zhongshan Hospital, Fudan University & Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, Shanghai, PR China. cui.jiefeng@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0001-6996-720X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82272959
6 · The paper itself

Abstract

Apart from the classic features, it is almost unknown whether there exist other new pathological features during pre-metastatic niche formation in hepatocellular carcinoma (HCC). Our previous works have highlighted the contribution of increased matrix stiffness to lung pre-metastatic niche formation and metastasis in HCC. However, whether increased matrix stiffness influences glucose metabolism and supply of lung pre-metastatic niche remains largely unclear. Here we uncover the underlying mechanism by which matrix stiffness-tuned exosomal miRNAs as the major contributor modulate glucose enrichment during lung pre-metastatic niche formation through decreasing the glucose uptake and consumption of lung fibroblasts and increasing angiogenesis and vascular permeability. Our findings suggest that glucose enrichment, a new characteristic of the lung pre-metastatic niche triggered by matrix stiffness-tuned exosomal miRNAs, is essential for the colonization and survival of metastatic tumor cells, as well as subsequent metastatic foci growth.

Indexed as

Carcinoma, HepatocellularExosomesExtracellular MatrixGlucoseLiver NeoplasmsLung NeoplasmsMicroRNAsAnimalsCell Line, TumorFibroblastsHumansLungMaleMiceNeovascularization, PathologicTumor MicroenvironmentGlucoseMicroRNAs

Identifiers

PMID39966385
PMCPMC11836368

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.