Evidence map›Paper›PMID 38450521›Full record

ArticleHaematologica2024

Small extracellular vesicles derived from acute myeloid leukemia cells promote leukemogenesis by transferring miR-221-3p.

Mengyu Li, Guohuan Sun, Jinlian Zhao, Shuangshuang Pu, Yanling Lv, Yifei Wang, Yapu Li, Xiangnan Zhao, Yajie Wang, Shangda Yang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 12 citations in OpenAlex.

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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

12 authors at 5 institutions in 2 countries.

Mengyu LiState Key Laboratory of Experimental Hematology; The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Department of Cell Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China; State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin.
Guohuan SunState Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China; CAMS Center for Stem Cell Medicine, PUMC Department of Stem Cell and Regenerative Medicine, Tianjin, China; Department of Stem Cell and Regenerative Medicine, Peking Union Medical College, Tianjin.
Jinlian ZhaoDepartment of Hematology, National Key Clinical Specialty of Hematology, Yunnan Blood Disease Clinical Medical Center, Yunnan Blood Disease Hospital, The First People's Hospital of Yunnan Province, Kunming.
Shuangshuang PuState Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematologyand Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China; CAMS Center for Stem Cell Medicine, PUMC Department of Stem Cell and Regenerative Medicine, Tianjin, China; Department of Stem Cell and Regenerative Medicine, Peking Union Medical College, Tianjin.
Yanling LvState Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin.
Yifei WangState Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin.
Yapu LiState Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China; CAMS Center for Stem Cell Medicine, PUMC Department of Stem Cell and Regenerative Medicine, Tianjin, China; Department of Stem Cell and Regenerative Medicine, Peking Union Medical College, Tianjin.
Xiangnan ZhaoState Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China; CAMS Center for Stem Cell Medicine, PUMC Department of Stem Cell and Regenerative Medicine, Tianjin, China; Department of Stem Celland Regenerative Medicine, Peking Union Medical College, Tianjin.
Yajie WangDepartment of Hematology, National Key Clinical Specialty of Hematology, Yunnan Blood Disease Clinical Medical Center, Yunnan Blood Disease Hospital, The First People's Hospital of Yunnan Province, Kunming. kbb165wyj@sina.com.
Shangda YangState Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China; CAMS Center for Stem Cell Medicine, PUMC Department of Stem Cell and Regenerative Medicine, Tianjin, China; Department of Stem Cell and Regenerative Medicine, Peking Union Medical College, Tianjin. yangshangda@ihcams.ac.cn.
Tao ChengState Key Laboratory of Experimental Hematology; The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Department of Cell Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China; State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China; CAMS Center for Stem Cell Medicine, PUMC Department of Stem Cell and Regenerative Medicine, Tianjin, China; Department of Stem Cell and Regenerative Medicine, Peking Union Medical College, Tianjin. chengtao@ihcams.ac.cn.
Hui ChengState Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China; CAMS Center for Stem Cell Medicine, PUMC Department of Stem Cell and Regenerative Medicine, Tianjin, China; Department of Stem Cell and Regenerative Medicine, Peking Union Medical College, Tianjin. chenghui@ihcams.ac.cn.
Institute of Hematology & Blood Diseases Hospital · CNPeking Union Medical College Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNFirst People's Hospital of Yunnan Province · CNNational Clinical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small extracellular vesicles (sEV) transfer cargos between cells and participate in various physiological and pathological processes through their autocrine and paracrine effects. However, the pathological mechanisms employed by sEV-encapsulated microRNA (miRNA) in acute myeloid leukemia (AML) are still obscure. In this study, we aimed to investigate the effects of AML cell-derived sEV (AML-sEV) on AML cells and delineate the underlying mechanisms. We initially used high-throughput sequencing to identify miR-221-3p as the miRNA prominently enriched in AML-sEV. Our findings revealed that miR-221-3p promoted AML cell proliferation and leukemogenesis by accelerating cell cycle entry and inhibiting apoptosis. Furthermore, Gbp2 was confirmed as a target gene of miR-221-3p by dual luciferase reporter assays and rescue experiments. Additionally, AML-sEV impaired the clonogenicity, particularly the erythroid differentiation ability, of hematopoietic stem and progenitor cells. Taken together, our findings reveal how sEV-delivered miRNA contribute to AML pathogenesis, which can be exploited as a potential therapeutic target to attenuate AML progression.

Indexed as

Cell ProliferationExtracellular VesiclesLeukemia, Myeloid, AcuteMicroRNAsAnimalsApoptosisCell DifferentiationCell Line, TumorCell Transformation, NeoplasticGene Expression Regulation, LeukemicHumansMiceMicroRNAsMIR221, human

Identifiers

PMID38450521
PMCPMC11443396
OpenAlexW4392557112

What OpenQuestion holds

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LicenceCC BY-NC
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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.