Evidence map›Paper›PMID 32396269›Full record

ArticleJournal of cellular and molecular medicine2020

Lung CSC-derived exosomal miR-210-3p contributes to a pro-metastatic phenotype in lung cancer by targeting FGFRL1.

Li Wang, Jun He, Haoyue Hu, Li Tu, Zhen Sun, Yanyang Liu, Feng Luo

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

68 citing papers in PubMed, 102 citations in OpenAlex.

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  16. Exosomal microRNAs: impact on cancer detection, treatment, and monitoring.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025
    Review
  17. Regulation of Cancer Stem Cells in the Tumor Microenvironment.Cancer heterogeneity and plasticity · 2025
    Article
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8 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

7 authors at 1 institution in 1 country.

Li WangLung Cancer Center, Cancer Center, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.ORCID 0000-0002-9270-4544
Jun HeLung Cancer Center, Cancer Center, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Haoyue HuLung Cancer Center, Cancer Center, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Li TuLung Cancer Center, Cancer Center, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Zhen SunLaboratory of Experimental Oncology, State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.ORCID 0000-0003-3374-480X
Yanyang LiuLung Cancer Center, Cancer Center, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Feng LuoLung Cancer Center, Cancer Center, and State Key Laboratory of Biotherapy, West China Hospital of Sichuan University, Chengdu, China.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer has the highest mortality rate among human cancers, and the majority of deaths can be attributed to metastatic spread. Lung cancer stem cells (CSCs) are a component of the tumour microenvironment that contributes to this process. Exosomes are small membrane vesicles secreted by all types of cells that mediate cell interactions, including cancer metastasis. Here, we show that lung CSC-derived exosomes promote the migration and invasion of lung cancer cells, up-regulate expression levels of N-cadherin, vimentin, MMP-9 and MMP-1, and down-regulate E-cadherin expression. Moreover, we verified that these exosomes contribute to a pro-metastatic phenotype in lung cancer cells via miR-210-3p transfer. The results of bioinformatics analysis and dual-luciferase reporter assays further indicated that miR-210-3p may bind to fibroblast growth factor receptor-like 1 (FGFRL1); silencing FGFRL1 enhanced the metastatic ability of lung cancer cells, whereas overexpressing FGFRL1 suppressed metastasis. Taken together, our results provide new insights into a potential molecular mechanism whereby lung CSC-derived exosomal miR-210-3p targets FGFRL1 to promote lung cancer metastasis. FGFRL1 may be a promising therapeutic target in lung cancer.

Indexed as

Base SequenceCell Line, TumorEndocytosisExosomesGene Expression Regulation, NeoplasticGene SilencingHumansLung NeoplasmsMicroRNAsNeoplastic Stem CellsPhenotypeReceptor, Fibroblast Growth Factor, Type 5Spheroids, CellularFGFRL1 protein, humanMicroRNAsMIRN210 microRNA, humanReceptor, Fibroblast Growth Factor, Type 5exosomelung cancer stem cellmetastasismiR-210-3p

Identifiers

PMID32396269
PMCPMC7294132
OpenAlexW3025440864

What OpenQuestion holds

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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 OpenQuestion graph.