Evidence map›Paper›PMID 34074322›Full record

ArticleJournal of experimental & clinical cancer research : CR2021

Hypoxic tumor-derived exosomal miR-31-5p promotes lung adenocarcinoma metastasis by negatively regulating SATB2-reversed EMT and activating MEK/ERK signaling.

Fengqiang Yu, Mingqiang Liang, Yu Huang, Weidong Wu, Bin Zheng, Chun Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 100 citations in OpenAlex.

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  16. New roles of tumor-derived exosomes in tumor microenvironment.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024
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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

6 authors at 2 institutions in 1 country.

Fengqiang Yu *Department of Thoracic Surgery, Fujian Medical University Union Hospital, #29 Xinquan Road, 350001, Fuzhou, Fujian, China.
Mingqiang Liang *Department of Thoracic Surgery, Fujian Medical University Union Hospital, #29 Xinquan Road, 350001, Fuzhou, Fujian, China.
Yu HuangDepartment of Thoracic Surgery, Fujian Medical University Union Hospital, #29 Xinquan Road, 350001, Fuzhou, Fujian, China.
Weidong WuDepartment of Thoracic Surgery, Fujian Medical University Union Hospital, #29 Xinquan Road, 350001, Fuzhou, Fujian, China.
Bin ZhengDepartment of Thoracic Surgery, Fujian Medical University Union Hospital, #29 Xinquan Road, 350001, Fuzhou, Fujian, China.
Chun ChenDepartment of Thoracic Surgery, Fujian Medical University Union Hospital, #29 Xinquan Road, 350001, Fuzhou, Fujian, China. chenchun0209@163.com.
Fujian Medical University · CNUnion Hospital · CN

Funding

Science and Technology Major Project of Fujian province 2017YZ0001Startup Fund for scientific research, Fujian Medical University 2018QH2029
6 · The paper itself

Abstract

backgroundExosomes have emerged as critical mediators of intercellular communication. Hypoxia is widely recognized as a key regulator of tumor aggressiveness, and significantly affects exosome release by tumor cells. However, the effects of exosomes derived from hypoxic lung adenocarcinoma (LUAD) cells are poorly understood.

methodsSamples of miRNA isolated from hypoxic LUAD cell-derived exosomes (HExo) and normoxic LUAD cell-derived exosomes (NExo) were sequenced to identify miRNAs that might mediate tumor progression. Exosomal miRNA was co-cultured with LUAD cells to assess its biological effects on cell migration and metastasis both in vitro and in vivo. The cellular target of exosomal miRNA was confirmed by dual-luciferase assays. Western blot studies showed that exosomal miRNA regulated the related pathway. The availability of circulating exosomal miRNA derived from plasma was also evaluated.

resultsWe found that HExo could significantly enhance the migration and invasion of normoxic LUAD cells. MiRNA sequencing results suggested that miR-31-5p was largely internalized within HExo and could be taken up by normoxic LUAD cells. Exosomal miR-31-5p was found to directly target Special AT-Rich Sequence-Binding Protein 2 (SATB2)-revered epithelial mesenchymal transition and significantly increase activation of MEK/ERK signaling, thereby contributing to tumor progression both in vitro and in vivo. Furthermore, higher levels of circulating exosomal miR-31-5p were detected in LUAD patients, especially in patients with metastatic disease.

conclusionsOur findings demonstrate that exosomal miR-31-5p exerts a crucial role in LUAD progression, and could serve as a diagnostic biomarker for LUAD.

Indexed as

A549 CellsAdenocarcinoma of LungAnimalsCell MovementCell ProliferationCoculture TechniquesEpithelial-Mesenchymal TransitionExosomesGene Expression Regulation, NeoplasticHeterograftsHumansMAP Kinase Signaling SystemMatrix Attachment Region Binding ProteinsMiceMicroRNAsNeoplasm InvasivenessMatrix Attachment Region Binding ProteinsMicroRNAsMIRN31 microRNA, humanSATB2 protein, humanTranscription FactorsexosomehypoxiaLung adenocarcinomamiR-31-5pSATB2

Identifiers

PMID34074322
PMCPMC8167983
OpenAlexW3165413311

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.