Evidence map›Paper›PMID 40185722›Full record

ArticleCell death & disease2025

Cancer-associated fibroblasts secrete CSF3 to promote TNBC progression via enhancing PGM2L1-dependent glycolysis reprogramming.

Wenqi Qin, Bing Chen, Xin Li, Wenjing Zhao, Lijuan Wang, Ning Zhang, Xiaolong Wang, Dan Luo, Yiran Liang, Yaming Li and 3 more

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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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

13 authors.

Wenqi Qin *Department of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Bing Chen *Biological Resource Center, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Xin LiDepartment of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Wenjing ZhaoBiological Resource Center, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Lijuan WangBiological Resource Center, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.ORCID http://orcid.org/0000-0002-7885-9945
Ning ZhangDepartment of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Xiaolong WangDepartment of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Dan LuoDepartment of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Yiran LiangDepartment of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Yaming LiDepartment of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Xi ChenDepartment of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Tong ChenDepartment of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, PR China.
Qifeng YangDepartment of Breast Surgery, General Surgery, Qilu Hospital of Shandong University, Jinan, Shandong, PR China. qifengy_sdu@163.com.ORCID http://orcid.org/0000-0003-0576-8513

Funding

Natural Science Foundation of Shandong Province (Shandong Provincial Natural Science Foundation) ZR2022MH077
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is characterized by a pronounced hypoxic tumor microenvironment, with cancer-associated fibroblasts (CAFs) serving as the predominant cellular component and playing crucial roles in regulating tumor progression. However, the mechanism by which CAFs affect the biological behavior of tumor cells in hypoxic environment remain elusive. This study employed a bead-based multiplex immunoassay to analyze a panel of cytokines/chemokines and identified colony stimulating factor 3 (CSF3) as a significantly elevated component in the secretome of hypoxic CAFs. We found that CSF3 promoted the invasive behavior of TNBC cells by activating the downstream signaling pathway of its receptor, CSF3R. RNA sequencing analysis further revealed that phosphoglucomutase 2-like 1 (PGM2L1) is a downstream target of the CSF3/CSF3R signaling, enhancing the glycolysis pathway and providing energy to support the malignant phenotype of breast cancer. In vivo, we further confirmed that CSF3 promotes TNBC progression by targeting PGM2L1. These findings suggest that targeting CSF3/CSF3R may represent a potential therapeutic approach for TNBC.

Indexed as

Cancer-Associated FibroblastsGlycolysisPhosphoglucomutaseTriple Negative Breast NeoplasmsAnimalsCell Line, TumorDisease ProgressionFemaleHumansMiceMice, NudeReceptors, Colony-Stimulating FactorSignal TransductionTumor MicroenvironmentCSF3R protein, humanPhosphoglucomutaseReceptors, Colony-Stimulating Factor

Identifiers

PMID40185722
PMCPMC11971334

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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.