Evidence map›Paper›PMID 39036079›Full record

ArticleBioengineering & translational medicine2024

Engineered in vivo and in vitro tumor model recapitulates vasculogenic mimicry signatures in melanoma.

Qizhi Shuai, Xinrui Xu, Yuxiang Liang, Zulala Halbiyat, Xin Lu, Zixuan Hu, Zhiwei Peng, Jie An, Zhiwei Feng, Tingjuan Huang and 4 more

Abstract read
In one paragraph

Article in Bioengineering & translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. 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

14 authors.

Qizhi ShuaiDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.ORCID https://orcid.org/0000-0002-5284-0672
Xinrui XuDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.
Yuxiang LiangDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.
Zulala HalbiyatDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.
Xin LuDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.
Zixuan HuDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.
Zhiwei PengDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.
Jie AnDepartment of Nuclear Medicine The First Hospital of Shanxi Medical University, Collaborative Innovation Center for Molecular Imaging of Precision Medicine, Shanxi Medical University Taiyuan China.
Zhiwei FengDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.
Tingjuan HuangDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.ORCID https://orcid.org/0000-0003-3879-3117
Hong ZhaoDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.
Zhizhen LiuDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.
Jun XuDepartment of Hepatopancreatobiliary Surgery The First Hospital of Shanxi Medical University Taiyuan China.
Jun XieDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth Defect and Cell Regeneration, MOE Key Laboratory of Coal Environmental Pathogenicity and Prevention Shanxi Medical University Taiyuan China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vasculogenic mimicry (VM) describes a process by which tumor cells formed a novel microcirculation pattern in an endothelial cell-free manner. Clinically, VM is associated with aggressive phenotype and poor patient survival. However, the current models for investigating VM include 2D monolayer cultures, Matrigel-based cultures, and animal models, each of which has limitations. Matrigel-based models often exhibit batch-to-batch variations, while in vivo tumor models currently produce insufficient amounts of VM. There is currently no suitable tumor model to discover new therapeutic targets against VM. Herein, we establish an extracellular matrix (ECM)-based engineered tumor model in vivo and in vitro. In this study, we demonstrate that matrix proteins enhanced the VM formation in the engineered xenograft model. Furthermore, we also investigated the role of collagen/fibronectin (FN) in melanoma progression and VM formation. Compared with cells cultured on TCPS plates, the B16F10 cells cultured on collagen/FN coated plates showed increased proliferation and stemness, and significantly enhanced invasion and formation of VM networks. Molecular mechanism analysis showed that Integrin/VE-cadherin/EphA2/PI3K/MMP-2 signaling pathways are responsible for VM formation. Our results indicate that collagen/FN matrix plays an important role in VM formation in melanoma, suggesting that ECM protein is a potential therapeutic target for anti-VM therapy for melanoma.

Indexed as

extracellular matrixmelanomatumor modelvasculogenic mimicry

Identifiers

PMID39036079
PMCPMC11256191

What Socratic 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 Socratic graph.