Evidence map›Paper›PMID 36465358›Full record

ArticleFrontiers in oncology2022

TGF-β1 promotes human breast cancer angiogenesis and malignant behavior by regulating endothelial-mesenchymal transition.

Zi-Xiong Li, Jie-Xin Chen, Ze-Jun Zheng, Wang-Jing Cai, Xiong-Bin Yang, Yuan-Yuan Huang, Yao Gong, Feng Xu, Yong-Song Chen, Ling Lin

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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  8. Angiogenesis: Biological Mechanisms and In Vitro Models.Annals of biomedical engineering · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Zi-Xiong LiDepartment of Rheumatology and Immunology, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Jie-Xin ChenDepartment of Rheumatology and Immunology, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Ze-Jun ZhengDepartment of Rheumatology and Immunology, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Wang-Jing CaiDepartment of Rheumatology and Immunology, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Xiong-Bin YangDepartment of Rheumatology and Immunology, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Yuan-Yuan HuangDepartment of Rheumatology and Immunology, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Yao GongDepartment of Rheumatology, Shantou University Medical College, Shantou, China.
Feng XuDepartment of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Yong-Song ChenDepartment of Endocrinology, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
Ling LinDepartment of Rheumatology and Immunology, The First Affiliated Hospital of Shantou University Medical College, Shantou, China.
First Affiliated Hospital of Shantou University Medical College · CNShantou University · CNShantou University Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Endothelial-mesenchymal transition (EndMT) is an important process of angiogenesis, which plays a significant role in in tumor invasion and metastasis, while its regulatory mechanisms in breast cancer remain to be fully elucidated. We previously demonstrated that tumor-associated macrophages (TAMs) can induce EndMT in endothelial cells by secreting CCL18 through the activation of the TGF-β and Notch signaling pathways in breast cancer. This study was designed to study the role of EndMT in breast cancer angiogenesis and progression in order to explore the underlying mechanism. Methods: Immunohistochemistry (IHC) was used to evaluate the expression of microvascular density (MVD) and EndMT markers in breast cancer. TGF-β1 was used to induce EndMT models of differentiated-endothelial breast cancer stem-like cells (BCSLCs). Results: In this study, we demonstrated that the EndMT markers were positively associated with MVD indicating unfavorable prognosis of invasive ductal carcinoma (IDC) patients. Functionally, TGF-β1 promoted migration, proliferation and angiogenesis of differentiated-endothelial BCSLCs by inducing EndMT Conclusion: Our findings elucidated the mechanism of TGF-β1 in the promotion of angiogenesis and progression by EndMT in breast cancer.

Indexed as

angiogenesisBCSLCbreast cancerdorsal skinfold window chamberEndMTTGF-β1

Identifiers

PMID36465358
PMCPMC9709251
OpenAlexW4309310077

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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 OpenQuestion graph.