Evidence map›Paper›PMID 34497265›Full record

ArticleCell death & disease2021

Tumor-derived exosomal miR-3157-3p promotes angiogenesis, vascular permeability and metastasis by targeting TIMP/KLF2 in non-small cell lung cancer.

Zijian Ma, Ke Wei, Fengming Yang, Zizhang Guo, Chunfeng Pan, Yaozhou He, Jun Wang, Zhihua Li, Liang Chen, YiJiang Chen and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
5.9field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 101 citations in OpenAlex.

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19 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Zijian Ma *Department of Thoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Ke Wei *Department of Thoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.ORCID 0000-0001-5225-1109
Fengming Yang *Department of Medical Oncology, Key Laboratory of Cancer Prevention and Intervention, Ministry of Education, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Zizhang Guo *Department of Thoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Chunfeng PanDepartment of Thoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Yaozhou HeDepartment of Thoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Jun WangDepartment of Thoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Zhihua LiDepartment of Thoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Liang ChenDepartment of Thoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
YiJiang ChenDepartment of Thoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China. chenyjnjmu@163.com.
Yang XiaDepartment of Thoracic Surgery, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China. xiayang-1019@163.com.
Nanjing Medical University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastasis is the main cause of death in patients with advanced lung cancer. The exosomes released by cancer cells create tumor microenvironment, and then accelerate tumor metastasis. Cancer-derived exosomes are considered to be the main driving force for metastasis niche formation at foreign sites, but the mechanism in Non-small cell lung carcinoma (NSCLC) is unclear. In metastatic NSCLC patients, the expression level of miR-3157-3p in circulating exosomes was significantly higher than that of non-metastatic NSCLC patients. Here, we found that miR-3157-3p can be transferred from NSCLC cells to vascular endothelial cells through exosomes. Our work indicates that exosome miR-3157-3p is involved in the formation of pre-metastatic niche formation before tumor metastasis and may be used as a blood-based biomarker for NSCLC metastasis. Exosome miR-3157-3p has regulated the expression of VEGF/MMP2/MMP9 and occludin in endothelial cells by targeting TIMP/KLF2, thereby promoted angiogenesis and increased vascular permeability. In addition, exosome miR-3157-3p promoted the metastasis of NSCLC in vivo.

Indexed as

Base SequenceBiomarkers, TumorCapillary PermeabilityCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationExosomesGene Expression Regulation, NeoplasticHumansHuman Umbilical Vein Endothelial CellsKruppel-Like Transcription FactorsLung NeoplasmsMicroRNAsNeoplasm MetastasisNeovascularization, PathologicBiomarkers, TumorKLF2 protein, humanKruppel-Like Transcription FactorsMicroRNAsMIRN3157 microRNA, humanTissue Inhibitor of Metalloproteinase-2

Identifiers

PMID34497265
PMCPMC8426367
OpenAlexW3197901743

What OpenQuestion holds

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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.