PMN-MDSCs-derived exosomal S100A9 drives breast cancer progression by enhancing cancer stemness and CXCL5-mediated metastatic potential.

Bo Wang, Binjie Su, Qi Cai, Tao Jiang, Weidong Liu, Xiaoguo Zhao, Yuekang Xu, Changying Guo, Jinyao Li

Abstract read

In one paragraph

Article in Cell death discovery, 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

9 authors.

Bo WangXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, China.ORCID http://orcid.org/0009-0009-9112-3025

Binjie SuXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, China.

Qi CaiXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, China.

Tao JiangLaboratory Animal Center, Science and Technology Innovation and Transformation Service Center, Xinjiang Medical University, Urumqi, China.

Weidong LiuDepartment of Gastroenterology, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, China.

Xiaoguo ZhaoLaboratory Animal Center, Science and Technology Innovation and Transformation Service Center, Xinjiang Medical University, Urumqi, China.

Yuekang XuXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, China. yuekang.xu@hotmail.com.ORCID http://orcid.org/0000-0002-1100-3982

Changying GuoXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, China. guocha@xju.edu.cn.ORCID http://orcid.org/0000-0002-7992-565X

Jinyao LiXinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, China. ljyxju@xju.edu.cn.ORCID http://orcid.org/0000-0002-3295-6096

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32370627

6 · The paper itself

Abstract

Polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) represent a critical subset of immunosuppressive cells within the tumor microenvironment. Their interaction with breast cancer stem cells (BCSCs) constitutes a vital link that drives the malignant progression of breast cancer, particularly in triple-negative breast cancer (TNBC). However, the precise molecular mechanisms through which these cells mediate BCSC-related stemness reprogramming and enhanced metastatic potential in breast cancer remain inadequately understood. In this study, PMN-MDSCs were isolated from mouse breast cancer solid tumor tissues. Functional characterization was conducted using flow cytometric phenotyping, nuclear morphology analysis, and T cell immunosuppressive function assays. In vivo tumorigenesis experiments confirmed their pro-tumor growth effects and enhanced tumor stem cell characteristics. Concurrently, the CD44

Identifiers

PMID42151127

DOI10.1038/s41420-026-03134-7

PMCPMC13346805

What OpenQuestion holds

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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.