Evidence map›Paper›PMID 42249398›Full record

ArticleJournal of nanobiotechnology2026

The exosomal miRNA/FOXN3 axis empowers fibroblasts with tumor-promoting functions via enhanced migration and altered secretome.

Jian Zhang, Meng Li, Qian Li, Bin Fu, Yangyang Li, Shuangli Mi

Abstract read
In one paragraph

Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Jian ZhangBeijing Institute of Genomics, Chinese Academy of Sciences/China National Center for Bioinformation, Beijing, 100101, China.
Meng LiBeijing Institute of Genomics, Chinese Academy of Sciences/China National Center for Bioinformation, Beijing, 100101, China.
Qian LiBeijing Institute of Genomics, Chinese Academy of Sciences/China National Center for Bioinformation, Beijing, 100101, China.
Bin FuState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Yangyang LiBeijing Institute of Genomics, Chinese Academy of Sciences/China National Center for Bioinformation, Beijing, 100101, China.
Shuangli MiBeijing Institute of Genomics, Chinese Academy of Sciences/China National Center for Bioinformation, Beijing, 100101, China. mishl@big.ac.cn.

Funding

Noncommunicable Chronic Diseases-National Science and Technology Major Project 2025ZD0552004the Beijing Municipal Natural Science Foundation Z210011the Open Project Program of the State Key Laboratory of Medical Proteomics (Academy of Military Medical Sciences) SKLP-O202202the Science & Technology Development Fund of Tianjin Education Commission for Higher Education 2021KJ202the Strategic Priority Research Program of Chinese Academy of Sciences XDA0460202the Tianjin Key Medical Discipline Construction Project TJYXZDXK-3-003A
6 · The paper itself

Abstract

Malignant tumor tissues with high proliferative activity are frequently characterized by a rich abundance of cancer-associated fibroblasts (CAFs). Nevertheless, the precise molecular mechanisms by which CAF-tumor cell crosstalk drives malignant proliferation remain incompletely elucidated. In this study, we demonstrate that exosomal microRNAs derived from lung adenocarcinoma cells reprogram adjacent normal fibroblasts into CAFs through downregulation of their common target, FOXN3. Suppression of this transcriptional repressor enhances the expression of genes associated with cell migration and extracellular matrix remodeling, thereby potentiating CAF infiltration into the tumor core. The consequent spatial proximity between CAFs and tumor cells enables the aberrantly altered secretome of CAFs to exert robust paracrine effects on malignancy. By focusing on receptors that interact with these dysregulated secreted proteins, we evaluated the drug sensitivity of patients bearing highly proliferative tumors to receptor-targeting agents, revealing potential therapeutic opportunities. Collectively, our work offers a detailed molecular dissection of tumor cell proliferation and proposes translationally relevant strategies for cancer therapy.

Indexed as

Cancer-Associated FibroblastsExosomesForkhead Transcription FactorsMicroRNAsSecretomeAdenocarcinoma of LungAnimalsCell Line, TumorCell MovementCell ProliferationFibroblastsGene Expression Regulation, NeoplasticHumansLung NeoplasmsTumor MicroenvironmentForkhead Transcription FactorsMicroRNAsCancer-associated fibroblastsExosomeFOXN3Lung adenocarcinomaMalignant proliferationMicroenvironmentStroma

Identifiers

PMID42249398
PMCPMC13459620

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.