Evidence map›Paper›PMID 33350586›Full record

ArticleJournal of cellular and molecular medicine2021

Extracellular vesicles-encapsulated let-7i shed from bone mesenchymal stem cells suppress lung cancer via KDM3A/DCLK1/FXYD3 axis.

Jiefeng Liu, Yuhua Feng, Xinyu Zeng, Miao He, Yujing Gong, Yiping Liu

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

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

42 citing papers in PubMed, 57 citations in OpenAlex.

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  19. Bone-organ axes: bidirectional crosstalk.Military Medical Research · 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.

Jiefeng LiuDepartment of General Surgery, The Fourth Hospital of Changsha, Hunan Normal University, Changsha, China.
Yuhua FengDepartment of Oncology, the Second Xiangya Hospital, Central South University, Changsha, China.
Xinyu ZengDepartment of General Surgery, The Fourth Hospital of Changsha, Hunan Normal University, Changsha, China.
Miao HeDepartment of General Surgery, The Fourth Hospital of Changsha, Hunan Normal University, Changsha, China.
Yujing GongDepartment of General Surgery, The Fourth Hospital of Changsha, Hunan Normal University, Changsha, China.
Yiping LiuDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, China.ORCID 0000-0001-8680-9449
Hunan Normal University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence has suggested that extracellular vesicles (EVs) play a crucial role in lung cancer treatment. Thus, we aimed to investigate the modulatory role of bone marrow mesenchymal stem cell (BMSC)-EV-derived let-7i and their molecular mechanism in lung cancer progression. Microarray-based analysis was applied to predict lung cancer-related miRNAs and their downstream genes. RT-qPCR and Western blot analyses were conducted to determine Let-7i, lysine demethylase 3A (KDM3A), doublecortin-like kinase 1 (DCLK1) and FXYD domain-containing ion transport regulator 3 (FXYD3) expressions, after which dual-luciferase reporter gene assay and ChIP assay were used to identify the relationship among them. After loss- and gain-of-function assays, the effects of let-7i, KDM3A, DCLK1 and FXYD3 on the biological characteristics of lung cancer cells were assessed. Finally, tumour growth in nude mice was assessed by xenograft tumours in nude mice. Bioinformatics analysis screened out the let-7i and its downstream gene, that is KDM3A. The findings showed the presence of a high expression of KDM3A and DCLK1 and reduced expression of let-7i and FXYD3 in lung cancer. KDM3A elevated DCLK1 by removing the methylation of H3K9me2. Moreover, DCLK1 suppressed the FXYD3 expression. BMSC-EV-derived let-7i resulted in the down-regulation of KDM3A expression and reversed its promoting role in lung cancer development. Consistently, in vivo experiments in nude mice also confirmed that tumour growth was suppressed by the BMSC-EV-derived let-7i. In conclusion, our findings demonstrated that the BMSC-EV-derived let-7i possesses an inhibitory role in lung cancer progression through the KDM3A/DCLK1/FXYD3 axis, suggesting a new molecular target for lung cancer treatment.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionAdultAgedAnimalsCell Line, TumorDisease Models, AnimalDoublecortin-Like KinasesExtracellular VesiclesFemaleHeterograftsHistonesHumansIntracellular Signaling Peptides and ProteinsJumonji Domain-Containing Histone DemethylasesLung NeoplasmsDCLK1 protein, humanDoublecortin-Like KinasesFXYD3 protein, humanHistonesIntracellular Signaling Peptides and ProteinsJumonji Domain-Containing Histone DemethylasesKDM3A protein, humanMembrane ProteinsMicroRNAsmirnlet7 microRNA, humanNeoplasm ProteinsProtein Serine-Threonine Kinasesbone marrow mesenchymal stem celldoublecortin-like kinase 1extracellular vesiclesFXYD domain-containing ion transport regulator 3let-7ilung cancerlysine demethylase 3A

Identifiers

PMID33350586
PMCPMC7882949
OpenAlexW3115223552

What OpenQuestion 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 OpenQuestion graph.