Evidence map›Paper›PMID 39137404›Full record

ArticleCancer research2024

YAP1 Inhibition Induces Phenotype Switching of Cancer-Associated Fibroblasts to Tumor Suppressive in Prostate Cancer.

Hongtao Song, Tong Lu, Donghui Han, Jiayu Zhang, Lunbiao Gan, Chao Xu, Shaojie Liu, Peng Li, Keying Zhang, Zhihao Hu and 9 more

Abstract read
In one paragraph

Article in Cancer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing 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

53 citing papers in PubMed.

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  9. Heterogeneity of cancer-associated fibroblast subtypes in the prostate cancer microenvironment and their clinical implications: prognostic model construction and therapeutic target exploration based on bioinformatics analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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

19 authors.

Hongtao Song *Department of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0009-0007-4113-7432
Tong Lu *Department of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0001-5691-9209
Donghui Han *Department of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-3742-4355
Jiayu Zhang *Department of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-6898-6844
Lunbiao GanInstitute of Medical Research, Northwestern Polytechnical University, Xi'an, China.ORCID 0009-0009-4394-0565
Chao XuDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0001-8462-8337
Shaojie LiuDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-5706-3841
Peng LiDivision of Cancer Biology, Laboratory Animal Center, Fourth Military Medical University, Xi'an, China.ORCID 0009-0005-1864-5186
Keying ZhangDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-4615-1782
Zhihao HuDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0009-0005-0565-9052
Hongji LiDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0009-0005-7694-1880
Yu LiDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-6273-876X
Xiaolong ZhaoDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-7525-385X
Jingliang ZhangDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-2132-3621
Nianzeng XingDepartment of Urology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0008-2463-8021
Changhong ShiDivision of Cancer Biology, Laboratory Animal Center, Fourth Military Medical University, Xi'an, China.ORCID 0000-0001-7490-3593
Weihong WenInstitute of Medical Research, Northwestern Polytechnical University, Xi'an, China.ORCID 0000-0003-4739-4871
Fa YangDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0003-3091-3954
Weijun QinDepartment of Urology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.ORCID 0000-0002-7509-7164

Funding

National Natural Science Foundation of China (NSFC) 82173204National Natural Science Foundation of China (NSFC) 82202933National Natural Science Foundation of China (NSFC) 82203633National Natural Science Foundation of China (NSFC) 82220108004
6 · The paper itself

Abstract

Prostate cancer rarely responds to immune-checkpoint blockade (ICB) therapies. Cancer-associated fibroblasts (CAF) are critical components of the immunologically "cold" tumor microenvironment and are considered a promising target to enhance the immunotherapy response. In this study, we aimed to reveal the mechanisms regulating CAF plasticity to identify potential strategies to switch CAFs from protumorigenic to antitumor phenotypes and to enhance ICB efficacy in prostate cancer. Integration of four prostate cancer single-cell RNA sequencing datasets defined protumorigenic and antitumor CAFs, and RNA-seq, flow cytometry, and a prostate cancer organoid model demonstrated the functions of two CAF subtypes. Extracellular matrix-associated CAFs (ECM-CAF) promoted collagen deposition and cancer cell progression, and lymphocyte-associated CAFs (Lym-CAF) exhibited an antitumor phenotype and induced the infiltration and activation of CD8+ T cells. YAP1 activity regulated the ECM-CAF phenotype, and YAP1 silencing promoted switching to Lym-CAFs. NF-κB p65 was the core transcription factor in the Lym-CAF subset, and YAP1 inhibited nuclear translocation of p65. Selective depletion of YAP1 in ECM-CAFs in vivo promoted CD8+ T-cell infiltration and activation and enhanced the therapeutic effects of anti-PD-1 treatment on prostate cancer. Overall, this study revealed a mechanism regulating CAF identity in prostate cancer and highlighted a therapeutic strategy for altering the CAF subtype to suppress tumor growth and increase sensitivity to ICB. Significance: YAP1 regulates cancer-associated fibroblast phenotypes and can be targeted to switch cancer-associated fibroblasts from a protumorigenic subtype that promotes extracellular matrix deposition to a tumor-suppressive subtype that stimulates antitumor immunity and immunotherapy efficacy.

Indexed as

Adaptor Proteins, Signal TransducingCancer-Associated FibroblastsPhenotypeProstatic NeoplasmsTumor MicroenvironmentYAP-Signaling ProteinsAnimalsCD8-Positive T-LymphocytesCell Line, TumorExtracellular MatrixGene Expression Regulation, NeoplasticHumansImmune Checkpoint InhibitorsMaleMiceTranscription Factor RelAAdaptor Proteins, Signal TransducingImmune Checkpoint InhibitorsTranscription Factor RelATranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID39137404
PMCPMC11565174

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.