Evidence map›Paper›PMID 40411322›Full record

ArticleJournal of cellular and molecular medicine2025

The Combination of MIF Inhibitor and AEP Targeted Inhibitor to Reduce Lung Metastasis in Breast Cancer and Its Mechanism.

Junsong Chen, Wenke Xu, Luyang Meng, Xin Zhang, Mengyao Lin, Sheng Zhang, Yi Liu, Fang Guo

Abstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

8 authors.

Junsong ChenKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0003-1720-0802
Wenke XuKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Luyang MengDepartment of Vascular Surgery, Hangzhou Third People's Hospital, Hangzhou, Zhejiang, China.
Xin ZhangKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Mengyao LinKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.
Sheng ZhangDepartment of Pathology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Yi LiuDepartment of Radiotherapy, Huangpu Branch of the Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Fang GuoKey Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China.

Funding

the "111 Center" ZXQT626001The Fundamental Research Funds for the Central Universities 24X010201944The Special Fund for Basic Scientific Research of Central Colleges, Shanghai Jiaotong University for Nationalities' 17X100040081
6 · The paper itself

Abstract

Breast cancer, the most prevalent malignant tumour in women, is characterised by high metastatic potential and frequent recurrence, both of which significantly impact patient prognosis following metastasis. To address this challenge, identifying novel therapeutic target combinations is critical for improving metastatic breast cancer treatment. This study investigates the mechanism by which asparaginyl endopeptidase (AEP) regulates breast cancer metastasis. Bioinformatics analysis revealed a potential interaction between AEP and CD74, which was subsequently confirmed through co-immunoprecipitation (co-IP) experiments. Further investigations demonstrated that AEP activates ERK pathway phosphorylation via CD74 regulation, thereby enhancing epithelial-mesenchymal transition (EMT) progression and promoting breast cancer cell migration. Compared to controls, dual inhibition of AEP and CD74 effectively reduced EMT markers and the migratory capacity of cancer cells in vitro. Subsequent in vivo experiments showed that this combinatorial strategy significantly suppressed breast cancer lung metastasis in mice without observable toxicity. These findings elucidate the molecular mechanism through which AEP promotes metastasis via CD74 regulation, while validating the therapeutic efficacy and safety of dual AEP/CD74 targeting. This study provides a novel conceptual framework and potential therapeutic targets for metastatic breast cancer intervention.

Indexed as

Breast NeoplasmsIntramolecular OxidoreductasesLung NeoplasmsMacrophage Migration-Inhibitory FactorsAnimalsAntigens, Differentiation, B-LymphocyteAsparaginyl EndopeptidaseCell Line, TumorCell MovementCysteine EndopeptidasesEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistocompatibility Antigens Class IIHumansMiceAntigens, Differentiation, B-LymphocyteAsparaginyl EndopeptidaseCysteine EndopeptidasesHistocompatibility Antigens Class IIIntramolecular Oxidoreductasesinvariant chainMacrophage Migration-Inhibitory FactorsMIF protein, humanasparagine endopeptidasebreast cancerCD74lung metastasismacrophage migration inhibitory factor

Identifiers

PMID40411322
PMCPMC12102665

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LicenceCC BY
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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.