Evidence map›Paper›PMID 41856970›Full record

ArticleCell death & disease2026

A feedback mechanism from prostate cancer cells to macrophages, reinforced by STAT1, regulates tumor progression and resistance to radiotherapy.

Jia-Yin Chen, Yu-Ting Xue, Bin Lin, Xu-Yun Huang, Fei Lin, Dong-Ning Chen, Wan-Jin Zhang, Yong Wei, Xue-Yi Xue, Qing-Shui Zheng and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2026. 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

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

1 citing paper in PubMed.

  1. 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

12 authors.

Jia-Yin Chen *Department of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Yu-Ting Xue *Department of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Bin Lin *Department of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Xu-Yun Huang *Department of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Fei LinDepartment of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID http://orcid.org/0000-0002-1571-6867
Dong-Ning ChenDepartment of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Wan-Jin ZhangDepartment of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Yong WeiDepartment of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID http://orcid.org/0000-0001-5324-3733
Xue-Yi XueDepartment of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID http://orcid.org/0000-0002-6461-7435
Qing-Shui ZhengDepartment of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID http://orcid.org/0000-0002-7426-6501
Zhi-Bin KeDepartment of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China. dr.urology@fjmu.edu.cn.ORCID http://orcid.org/0000-0002-7563-7781
Ning XuDepartment of Urology, Urology Research Institute, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China. drxun@fjmu.edu.cn.ORCID http://orcid.org/0000-0001-7909-7025

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The resistance to radiotherapy of prostate cancer is driven by interactions within the tumor microenvironment, particularly between prostate cancer cells and tumor-associated macrophages, however the underlying mechanisms remain poorly understood. In this study, we found that STAT1 enhanced the transcription of critical glycolytic enzymes, leading to an increase in lactate secretion from prostate cancer cells. Then, the lactate was transported to macrophages via the MCT1 transporter, activating the NFκB1 pathway, which subsequently promoted macrophage polarization to the M2 phenotype and activated the transcription of MCP-1. MCP-1 was secreted from macrophages interacted with the CCR2 receptor on prostate cancer cells, thereby activating the JAK/STAT1 pathway, ultimately contributing to the progression of prostate cancer and its resistance to radiotherapy. Taken together, our findings identified a STAT1/lactate/NFκB1/MCP-1 positive feedback mechanism as a driver of prostate cancer progression and resistance to radiotherapy that functioned by interaction to macrophages, which could be potential therapeutic targets for the advanced prostate cancer.

Indexed as

Feedback, PhysiologicalMacrophagesProstatic NeoplasmsRadiation ToleranceSTAT1 Transcription FactorAnimalsCell Line, TumorChemokine CCL2Disease ProgressionHumansLactic AcidMaleNF-kappa BSignal TransductionTumor MicroenvironmentChemokine CCL2Lactic AcidNF-kappa BSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID41856970
PMCPMC13018544

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.