Evidence map›Paper›PMID 39639765›Full record

ArticleCancer science2025

Cancer-associated fibroblast-derived MMP11 promotes tumor progression in pancreatic cancer.

Zhuoyin Wang, Xu Guo, Xinming Li, Jing Wang, Nengwei Zhang, Buhe Amin, Guangzhong Xu, Bin Zhu

Abstract read
In one paragraph

Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Article
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  6. Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026
    Review
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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

8 authors.

Zhuoyin WangDepartment of General Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.ORCID https://orcid.org/0000-0003-2458-7873
Xu GuoDepartment of General Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Xinming LiDepartment of General Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Jing WangDepartment of General Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Nengwei ZhangDepartment of General Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Buhe AminDepartment of General Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Guangzhong XuDepartment of General Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.
Bin ZhuDepartment of General Surgery, Beijing Shijitan Hospital, Capital Medical University, Beijing, China.

Funding

Chunhui Project Foundation of the Education Department of China HZKY20220055
6 · The paper itself

Abstract

Matrix metalloproteinase 11 (MMP11), a zinc-dependent endopeptidase involved in extracellular matrix degradation and remodeling, has been identified as a tumor promoter in multiple cancer types. However, its expression pattern and role in pancreatic ductal adenocarcinoma (PDAC) remain unclear. In this study, elevated MMP11 expression was identified in PDAC tissues and was associated with diminished survival. Integrated single-cell RNA sequencing and co-immunofluorescence staining revealed that MMP11 was predominantly expressed in cancer-associated fibroblasts (CAFs). Mechanistically, cancer cell-derived TGF-β1 mediated CAF activation via the pSmad2/3 pathway and accompanied by MMP11 production. Additionally, MMP11 knockdown in CAFs impaired the proliferative and invasive abilities of AsPC-1 and BxPC-3 cells in vitro; which could be rescued by adding recombinant MMP11. Similarly, co-injection of AsPC-1 cells with MMP11-knockdown CAFs into nude mice significantly suppressed tumor growth and liver metastasis compared with tumors bearing unmodified CAFs. Furthermore, we confirmed that CAF-derived MMP11 may drive the epithelial-mesenchymal transition process of PDAC cells to promote tumor invasion via the PI3K/AKT pathway rather than extracellular matrix remodeling. Collectively, we uncovered a crosstalk between cancer cells and CAFs mediated by TGF-β1 and MMP11 that drives the progression of PDAC.

Indexed as

Cancer-Associated FibroblastsCarcinoma, Pancreatic DuctalMatrix Metalloproteinase 11Pancreatic NeoplasmsAnimalsCell Line, TumorCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeNeoplasm InvasivenessMatrix Metalloproteinase 11MMP11 protein, humanPhosphatidylinositol 3-KinasesTGFB1 protein, humanTransforming Growth Factor beta1CAFsEMTMMP11PDACtumor progression

Identifiers

PMID39639765
PMCPMC11875780

What Socratic holds

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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.