Evidence map›Paper›PMID 37461061›Full record

ArticleJournal of translational medicine2023

TGF-β1 dominates stromal fibroblast-mediated EMT via the FAP/VCAN axis in bladder cancer cells.

Qinrong Ping, Chunhui Wang, Xin Cheng, Yiming Zhong, Ruping Yan, Meng Yang, Yunqiang Shi, Xiangmeng Li, Xiao Li, Wenwen Huang and 12 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
11.5field-weighted citation impact, top 1% of its field
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

45 citing papers in PubMed, 50 citations in OpenAlex.

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  11. Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026
    Review
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  19. CTHRC1Frontiers in immunology · 2026
    Article
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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

22 authors at 2 institutions in 1 country.

Qinrong Ping *Department of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Chunhui Wang *Department of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Xin Cheng *Kunming Medical University, Kunming, 650051, China.
Yiming ZhongDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Ruping YanDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, China.
Meng YangDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Yunqiang ShiDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Xiangmeng LiDepartment of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming, 650101, China.
Xiao LiKey Laboratory of Tumor Immunological Prevention and Treatment of Yunnan Provincial, Kunming, 650051, China.
Wenwen HuangKey Laboratory of Tumor Immunological Prevention and Treatment of Yunnan Provincial, Kunming, 650051, China.
Liqiong WangDepartment of Pathology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Xiaofang BiDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Libing HuDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Yang YangDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Yingbao WangDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Rui GongDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Jun TanDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Rui LiDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Hui LiDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Jian LiDepartment of Urology, Yan'an Hospital Affiliated to Kunming Medical University, Kunming, 650051, China.
Wenju WangKey Laboratory of Tumor Immunological Prevention and Treatment of Yunnan Provincial, Kunming, 650051, China. wangwenju_vip@hotmail.com.
Ruhong LiKey Laboratory of Tumor Immunological Prevention and Treatment of Yunnan Provincial, Kunming, 650051, China. lrh272@126.com.ORCID 0000-0003-2435-7760
Kunming Medical University · CNYunnan Center for Disease Control And Prevention · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBladder cancer is one of the most common malignant tumors of the urinary system and is associated with a poor prognosis once invasion and distant metastases occur. Epithelial-mesenchymal transition (EMT) drives metastasis and invasion in bladder cancer. Transforming growth factor β1 (TGF-β1) and stromal fibroblasts, especially cancer-associated fibroblasts (CAFs), are positive regulators of EMT in bladder cancer. However, it remains unclear how TGF-β1 mediates crosstalk between bladder cancer cells and CAFs and how it induces stromal fibroblast-mediated EMT in bladder cancer. We aimed to investigate the mechanism of TGF-β1 regulation of stromal fibroblast-mediated EMT in bladder cancer cells.

methodsPrimary CAFs with high expression of fibroblast activation protein (FAP) were isolated from bladder cancer tissue samples. Subsequently, different conditioned media were used to stimulate the bladder cancer cell line T24 in a co-culture system. Gene set enrichment analysis, a human cytokine antibody array, and cytological assays were performed to investigate the mechanism of TGF-β1 regulation of stromal fibroblast-mediated EMT in bladder cancer cells.

resultsAmong the TGF-β family, TGF-β1 was the most highly expressed factor in bladder cancer tissue and primary stromal fibroblast supernatant. In the tumor microenvironment, TGF-β1 was mainly derived from stromal fibroblasts, especially CAFs. In stimulated bladder cells, stromal fibroblast-derived TGF-β1 promoted bladder cancer cell migration, invasion, and EMT. Furthermore, TGF-β1 promoted the activation of stromal fibroblasts, inducing CAF-like features, by upregulating FAP in primary normal fibroblasts and a normal fibroblast cell line. Stromal fibroblast-mediated EMT was induced in bladder cancer cells by TGF-β1/FAP. Versican (VCAN), a downstream molecule of FAP, plays an essential role in TGF-β1/FAP axis-induced EMT in bladder cancer cells. VCAN may also function through the PI3K/AKT1 signaling pathway.

conclusionsTGF-β1 is a critical mediator of crosstalk between stromal fibroblasts and bladder cancer cells. We revealed a new mechanism whereby TGF-β1 dominated stromal fibroblast-mediated EMT of bladder cancer cells via the FAP/VCAN axis and identified potential biomarkers (FAP, VCAN, N-cadherin, and Vimentin) of bladder cancer. These results enhance our understanding of bladder cancer invasion and metastasis and provide potential strategies for diagnosis, treatment, and prognosis.

Indexed as

Transforming Growth Factor beta1Urinary Bladder NeoplasmsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFibroblast Activation Protein AlphaFibroblastsHumansSignal TransductionTumor MicroenvironmentUrinary BladderVersicansFibroblast Activation Protein AlphaTransforming Growth Factor beta1VCAN protein, humanVersicansBladder cancerEpithelial-mesenchymal transitionFibroblast activation proteinStromal fibroblastsTransforming growth factor β1Versican

Identifiers

PMID37461061
PMCPMC10351189
OpenAlexW4384558868

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.