Evidence map›Paper›PMID 33789743›Full record

ArticleExperimental hematology & oncology2021

Exosomes from BM-MSCs promote acute myeloid leukemia cell proliferation, invasion and chemoresistance via upregulation of S100A4.

Tianxin Lyu, Yinuo Wang, Ding Li, Hui Yang, Bin Qin, Wenli Zhang, Zhiyue Li, Cheng Cheng, Binglei Zhang, Rongqun Guo and 1 more

Open access · goldAbstract read
In one paragraph

Article in Experimental hematology & oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 71 citations in OpenAlex.

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  17. Regulation of Cancer Stem Cells in the Tumor Microenvironment.Cancer heterogeneity and plasticity · 2025
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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

11 authors at 3 institutions in 1 country.

Tianxin LyuDepartment of Hematology, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, 450008, China.
Yinuo WangTranslational Cancer Research Center, Peking University First Hospital, Beijing, 100034, China.
Ding LiDepartment of Pharmacy, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, 450008, China.
Hui YangTranslational Cancer Research Center, Peking University First Hospital, Beijing, 100034, China.
Bin QinAcademy of Medical Sciences, Zhengzhou University, Zhengzhou, 450052, China.
Wenli ZhangDepartment of Hematology, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, 450008, China.
Zhiyue LiDepartment of Hematology, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, 450008, China.
Cheng ChengDepartment of Hematology, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, 450008, China.
Binglei ZhangAcademy of Medical Sciences, Zhengzhou University, Zhengzhou, 450052, China.
Rongqun GuoDepartment of Hematology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Yongping SongDepartment of Hematology, Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, 450008, China. songyongping001@126.com.ORCID http://orcid.org/0000-0002-1659-7441
Zhengzhou University · CNPeking University · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

Henan Provincial Science and Technology Research Project 202102310157Medical Science and Technology Research Plan (Joint Construction) Project of Henan Province LHGJ20190676Medical Science and Technology Research Plan (Joint Construction) Project of Henan Province SBGJ2018085
6 · The paper itself

Abstract

backgroundBM-MSCs play an important role in cancer development through the release of cytokines or exosomes. Studies have shown that extracellular exosomes derived from BM-MSCs are a key pro-invasive factor. However, how BM-MSC-exos influence AML cell proliferation, invasion and chemoresistance remains poorly understood.

methodsWe isolated exosomes from BM-MSCs and used electron microscopy, particle size separation and western blots to identify the exosomes. The invasion of leukemia cells was observed with a transwell assay. The stemness traits and chemoresistance of the leukemia cells were detected by FCM, colony formation and CCK-8 assays. TCGA database was used to investigate the prognostic relevance of S100A4 and its potential role in AML.

resultsIn this study, we found that BM-MSC-exos increased the metastatic potential, maintained the stemness and contributed to the chemoresistance of leukemia cells. Mechanistically, BM-MSC-exos promoted the proliferation, invasion and chemoresistance of leukemia cells via upregulation of S100A4. Downregulating S100A4 clearly suppressed the proliferation, invasion, and chemoresistance of leukemia cells after treatment with BM-MSC-exos. Bioinformatic analysis with data in TCGA database showed that S100A4 was associated with poor prognosis in AML patients, and functional enrichment revealed its involvement in the processes of cell-cell adhesion and cytokine regulation.

conclusionsS100A4 is vital in the BM-MSC-exo-driven proliferation, invasion and chemoresistance of leukemia cells and may serve as a potential target for leukemia therapy.

Indexed as

Acute myeloid leukemiaChemoresistanceExosomeInvasionMesenchymal stem cells

Identifiers

PMID33789743
PMCPMC8011411
OpenAlexW3142408614

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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.