Evidence map›Paper›PMID 32317629›Full record

ArticleSignal transduction and targeted therapy2020

Exosomes with low miR-34c-3p expression promote invasion and migration of non-small cell lung cancer by upregulating integrin α2β1.

Wenjing Huang, Yanyan Yan, Yun Liu, Minting Lin, Jinxiang Ma, Wei Zhang, Jianwei Dai, Jiajun Li, Qiaoru Guo, Hubiao Chen and 5 more

Abstract read
In one paragraph

Article in Signal transduction and targeted therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing 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

84 citing papers in PubMed.

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  17. mMedComm · 2024
    Article
  18. Review
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24 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

15 authors.

Wenjing Huang *Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, 511436, Guangzhou, Guangdong, P.R. China.
Yanyan Yan *Institute of Respiratory and Occupational Diseases, Collaborative Innovation Center for Cancer, Medical College, Shanxi Datong University, 037009, Datong, P.R. China.
Yun Liu *Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, 511436, Guangzhou, Guangdong, P.R. China.
Minting Lin *Guangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, 511436, Guangzhou, Guangdong, P.R. China.
Jinxiang MaCollege of Public Health, Guangzhou Medical University, 511436, Guangzhou, Guangdong, P.R. China.
Wei ZhangCancer Center of Datong, the Second People's Hospital of Datong, 037005, Shanxi, P.R. China.
Jianwei DaiGZMU-GIBH School of Life Sciences, Guangzhou Medical University, 511436, Guangzhou, Guangdong, P.R. China.
Jiajun LiGuangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, 511436, Guangzhou, Guangdong, P.R. China.
Qiaoru GuoGuangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, 511436, Guangzhou, Guangdong, P.R. China.
Hubiao ChenSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong, P.R. China.
Bolat MakabelXinjiang Institute of Materia Medica, 830004, Urumqi, P.R. China.
Hong LiuInstitute of Respiratory and Occupational Diseases, Collaborative Innovation Center for Cancer, Medical College, Shanxi Datong University, 037009, Datong, P.R. China.
Chaoyue SuGuangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, 511436, Guangzhou, Guangdong, P.R. China.
Hong BiDepartment of Pathology, Shanxi Provincial People's Hospital, 030012, Taiyuan, P.R. China.
Jianye ZhangGuangdong Provincial Key Laboratory of Molecular Target & Clinical Pharmacology, School of Pharmaceutical Sciences and the Fifth Affiliated Hospital, Guangzhou Medical University, 511436, Guangzhou, Guangdong, P.R. China. jianyez@163.com.ORCID http://orcid.org/0000-0001-5242-3687

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exosomes play critical roles in regulating various physiological and pathological processes, including immune stimulation, immune suppression, cardiovascular diseases, and cancers. Recent studies show that exosomes that transport specific microRNAs (miRNAs) are involved in tumor development. However, the molecular mechanism by which tumor invasion and migration are regulated by exosomes from non-small cell lung cancer (NSCLC) is not well understood. Here, we show that exosomes shuttling low levels of miR-34c-3p are involved in NSCLC progression. Our results showed that exosomes derived from NSCLC cells carrying low levels of miR-34c-3p could be transported into the cytoplasm of NSCLC cells and accelerate NSCLC invasion and migration by upregulating integrin α2β1. A luciferase assay revealed that integrin α2β1 was the direct target of miR-34c-3p, and overexpression of integrin α2β1 could promote the invasion and migration of NSCLC cells. The analysis of exosomes derived from clinical serum samples indicated that the expression of miR-34c-3p was significantly downregulated in exosomes from NSCLC patients compared with that of normal controls. A549-derived exosomes promoted NSCLC cells lung metastases in vivo. Exosomes shuttling low levels of miR-34c-3p were associated with the progression of NSCLC in vitro and in vivo. Our data demonstrate that exosomes shuttling low levels of miR-34c-3p can accelerate the invasion and migration of NSCLC by upregulating integrin α2β1. MiR-34c-3p can be a diagnostic and prognostic marker for NSCLC. High expression of integrin α2β1 is positively related to the migration and metastasis of NSCLC cells.

Indexed as

A549 CellsAgedAnimalsCarcinoma, Non-Small-Cell LungCell MovementCell ProliferationExosomesFemaleGene Expression Regulation, NeoplasticHeterograftsHumansIntegrin alpha2beta1MaleMiceMicroRNAsMiddle AgedIntegrin alpha2beta1MicroRNAsMIRN34 microRNA, human

Identifiers

PMID32317629
PMCPMC7174429

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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.