Evidence map›Paper›PMID 41870750›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2026

CX3CL1-CX3CR1 signaling orchestrates malignant progression of prostate cancer through luminal progenitor-macrophage crosstalk.

Yu Jiang, Yuchen Guo, Lizhuang Han, Shiwei Wang, Fang Wang, Yongliang Zhao, Jiajia Wang, Junyan Han, Miaomiao Liu, Zhihua Liu and 1 more

Abstract read
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In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 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

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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

11 authors.

Yu Jiang *Biomedical Innovation Center, Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, China.
Yuchen Guo *National Clinical Research Center for Geriatric Diseases, Xuanwu Hospital of Capital Medical University, No. 45, Changchun Street, Xicheng District, Beijing, 100053, China.
Lizhuang HanBiomedical Innovation Center, Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, China.
Shiwei WangBiomedical Innovation Center, Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, China.
Fang WangBiomedical Innovation Center, Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, China.
Yongliang ZhaoSuzhou Xi'an Jiaotong-Liverpool Technology Transfer Center, Suzhou, 215009, China.
Jiajia WangBiomedical Innovation Center, Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, China.
Junyan HanBiomedical Innovation Center, Beijing Shijitan Hospital, Capital Medical University, Beijing, 100038, China.
Miaomiao LiuLaboratory Animal Resources Center, Tsinghua University, Beijing, 100084, China.
Zhihua LiuInstitute of Immunology, School of Basic Medicine, Tsinghua University, Medical Science Building, Haidian District, Beijing, 100084, China. zhihualiu@tsinghua.edu.cn.
Qin ZhangNational Clinical Research Center for Geriatric Diseases, Xuanwu Hospital of Capital Medical University, No. 45, Changchun Street, Xicheng District, Beijing, 100053, China. qinzhang@mail.ccmu.edu.cn.

Funding

Joint Research Center for Genomic Resources 2017B01012State Key Laboratory of Membrane Biology No.2025LMB006the National Natural Science Foundation of China No. 82270572
6 · The paper itself

Abstract

purposeProgression to castration-resistant prostate cancer (CRPC) is shaped by dynamic interactions within the tumor microenvironment (TME). However, the specific cellular crosstalk driving therapeutic resistance and metastasis remains incompletely defined. This study aims to identify key signaling axes between therapy-resistant luminal progenitor (luminal-2) cells and immune components in the TME, particularly tumor-associated macrophages (TAMs), and to determine how these interactions promote immunosuppression and cancer stem-like cell expansion during disease progression.

methodsWe employed an integrative phenomics approach combining single-cell transcriptomics with genetically engineered mouse models (GEMMs) and orthotopic allograft models of prostate cancer. Spatiotemporal changes in cell populations were profiled across disease stages. The functional contribution of the CX3CL1-CX3CR1 axis was evaluated through genetic ablation of Cx3cr1 in host mice, followed by assessment of TAM infiltration, luminal progenitor cell dynamics, tumor growth, and immunosuppression signature score.

resultsSingle-cell profiling revealed a distinct luminal-2 progenitor population with high CX3CL1 expression that recruits CX3CR1

conclusionThe CX3CL1-CX3CR1 axis functions as a critical mediator of reciprocal signaling between luminal-2 progenitors and TAMs that promotes immune evasion, stemness maintenance, and therapeutic resistance in prostate cancer. Disrupting this pathway impairs the pro-tumoral niche and may represent a promising therapeutic approach for advanced prostate cancer.

Indexed as

Chemokine CX3CL1CX3C Chemokine Receptor 1Disease ProgressionMacrophagesNeoplastic Stem CellsProstatic NeoplasmsSignal TransductionAnimalsCell Line, TumorHumansMaleMiceTumor-Associated MacrophagesTumor MicroenvironmentChemokine CX3CL1CX3C Chemokine Receptor 1Cx3cr1 protein, mouseCX3CL1-CX3CR1 axisLuminal progenitor cells (luminal 2 cells)Prostate cancerTumor-associated macrophages (TAMs)

Identifiers

PMID41870750
PMCPMC13009301

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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.