Evidence map›Paper›PMID 40817243›Full record

ArticleJournal of translational medicine2025

MRO/HNRNPU/CCL5 feedback loop amplifies M2 macrophage and breast cancer cell crosstalk to drive progression.

Zhirui Zeng, Xin Bao, Shan Lei, Wenjing Tang, Huading Tai, Lu Wang, Dahuan Li, Shu Liu, Tengxiang Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 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

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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

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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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

9 authors.

Zhirui Zeng *Engineering Research Center of Chronic Disease Diagnosis and Treatment, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou, 550009, China.
Xin Bao *Engineering Research Center of Chronic Disease Diagnosis and Treatment, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou, 550009, China.
Shan Lei *Engineering Research Center of Chronic Disease Diagnosis and Treatment, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou, 550009, China.
Wenjing TangEngineering Research Center of Chronic Disease Diagnosis and Treatment, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou, 550009, China.
Huading TaiEngineering Research Center of Chronic Disease Diagnosis and Treatment, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou, 550009, China.
Lu WangEngineering Research Center of Chronic Disease Diagnosis and Treatment, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou, 550009, China.
Dahuan LiEngineering Research Center of Chronic Disease Diagnosis and Treatment, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou, 550009, China. lidahuan@gmc.edu.cn.
Shu LiuDepartment of Breast Surgery, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, 550009, China. liushu@gmc.edu.cn.
Tengxiang ChenEngineering Research Center of Chronic Disease Diagnosis and Treatment, School of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou, 550009, China. txch@gme.edu.cn.

Funding

Affiliated Hospital of Guizhou Medical University Leading Scholar Project gyfykyc-2023-01Affiliated Hospital of Guizhou Medical University Postdoctoral fellow Start-up fund BSH-Q-2023-06Continuous Support Fund for Excellent Scientific Research Platform of Colleges and Universities in Guizhou Province QJJ (2022) 020Innovative Research Group Project of the National Natural Science Foundation of China 82303903Innovative Research Group Project of the National Natural Science Foundation of China 82473969National Natural Science Foundation Cultivation Project of the Affiliated Hospital of Guizhou Medical University gyfynsfc02021-4
6 · The paper itself

Abstract

backgroundM2 macrophages are known to enhance the malignant phenotype of breast cancer (BC) cells, yet the underlying mechanisms remain unclear.

methodsscRNA sequencing analysis, chromatin immunoprecipitation, immunoprecipitation, exosome isolation, and biological experiments were used to analyze this crosstalk.

resultsMaestro (MRO) was involved in the crosstalk between M2 macrophages and BC cells. MRO expression was elevated in BC tissues, particularly in those with high CD68 and CD206 expression, and correlated with poor prognosis. MRO was highly expressed in M2 macrophages, and its mRNA was transferred from M2 macrophages to BC cells via exosomes. Engineering exosomes with MRO knockdown demonstrated reduced tumor-promoting effects compared to controls. Mechanistically, MRO in BC cells functioned as a nuclear import protein, facilitating the translocation of HNRNPU into the nucleus. HNRNPU then enhanced CCL5 transcription by binding to its promoter. Elevated CCL5 not only promoted BC cell malignancy, but also recruited more macrophages and induced M2 polarization.

conclusionsThese findings reveal a novel MRO/HNRNPU/CCL5 feedback loop in the interaction between M2 macrophages and BC cells, driving BC progression and reshaping the tumor microenvironment. Targeting this feedback loop offers a potential therapeutic strategy for BC.

Indexed as

Breast NeoplasmsCell CommunicationChemokine CCL5Disease ProgressionFeedback, PhysiologicalMacrophagesAnimalsCell Line, TumorExosomesFemaleGene Expression Regulation, NeoplasticHumansTumor MicroenvironmentCCL5 protein, humanChemokine CCL5Breast cancerFeedback loopM2 macrophageMRO

Identifiers

PMID40817243
PMCPMC12355852

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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.