Evidence map›Paper›PMID 39115624›Full record

ArticleAngiogenesis2024

PDPN/CCL2/STAT3 feedback loop alter CAF heterogeneity to promote angiogenesis in colorectal cancer.

Die Yu, Hanzheng Xu, Jinzhe Zhou, Kai Fang, Zekun Zhao, Ke Xu

Abstract read
PubMed Publisher
In one paragraph

Article in Angiogenesis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Signaling pathways and targeted interventions for precancers.Signal transduction and targeted therapy · 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

6 authors.

Die Yu *State Key Laboratory of Bioreactor Engineering, Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, 130 Meilong Rd, Shanghai, 200237, China.
Hanzheng Xu *State Key Laboratory of Bioreactor Engineering, Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, 130 Meilong Rd, Shanghai, 200237, China.
Jinzhe Zhou *Department of General Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, 200065, China.
Kai FangState Key Laboratory of Bioreactor Engineering, Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, 130 Meilong Rd, Shanghai, 200237, China. fangkai94ok@163.com.
Zekun ZhaoDepartment of General Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, 200065, China. doctor999zack@163.com.
Ke XuInstitute of Translational Medicine, Shanghai University, Shanghai, 200444, China. kexu@shu.edu.cn.

Funding

Wenzhou Science and Technology Project No.Y20220178 & No.Y20220016
6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the common clinical malignancies and the fourth leading cause of cancer-related death in the world. The tumor microenvironment (TME) plays a crucial role in promoting tumor angiogenesis, and cancer-associated fibroblasts (CAFs) are one of the key components of the tumor microenvironment. However, due to the high heterogeneity of CAFs, elucidating the molecular mechanism of CAF-mediated tumor angiogenesis remained elusive. In our study, we found that there is pro-angiogenic functional heterogeneity of CAFs in colorectal cancer and we clarified that Podoplanin (PDPN) can specifically label CAF subpopulations with pro-angiogenic functions. We also revealed that PDPN + CAF could maintain CAF heterogeneity by forming a PDPN/CCL2/STAT3 feedback loop through autocrine CCL2, while activate STAT3 signaling pathway in endothelial cells to promote angiogenesis through paracrine CCL2. We demonstrated WP1066 could inhibit colorectal cancer angiogenesis by blocking both the PDPN/CCL2/STAT3 feedback loop in CAFs and the STAT3 signaling pathway in endothelial cells. Altogether, our study suggests that STAT3 could be a potential therapeutic target for blocking angiogenesis in colorectal cancer. We provide theoretical basis and new therapeutic strategies for the clinical treatment of colorectal cancer.

Indexed as

Cancer-Associated FibroblastsChemokine CCL2Colorectal NeoplasmsMembrane GlycoproteinsNeovascularization, PathologicSTAT3 Transcription FactorAngiogenesisAnimalsCell Line, TumorFeedback, PhysiologicalFemaleHumansHuman Umbilical Vein Endothelial CellsMaleMiceMice, NudeCCL2 protein, humanChemokine CCL2Membrane GlycoproteinsPDPN protein, humanPodoplaninSTAT3 protein, humanSTAT3 Transcription FactorAngiogenesisCAFCRCPDPNSTAT3

Identifiers

PMID39115624

What Socratic holds

Textmetadata
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.