Evidence map›Paper›PMID 35091542›Full record

ArticleCell death & disease2022

HucMSC exosomes promoted imatinib-induced apoptosis in K562-R cells via a miR-145a-5p/USP6/GLS1 axis.

Xiaowen Chen, Yixin Chen, Min Zhang, Hui Cheng, Huirong Mai, Meng Yi, Huanli Xu, Xiuli Yuan, Sixi Liu, Feiqiu Wen

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.6field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 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

10 authors at 3 institutions in 1 country.

Xiaowen Chen *Department of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen, 518038, China.
Yixin Chen *Department of Oncology, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, 518020, China.
Min ZhangDepartment of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen, 518038, China.
Hui ChengDepartment of Hematology, Changhai Hospital, Naval Military Medical University, Shanghai, 200433, China.ORCID http://orcid.org/0000-0001-9154-9282
Huirong MaiDepartment of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen, 518038, China.
Meng YiDepartment of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen, 518038, China.
Huanli XuDepartment of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen, 518038, China.
Xiuli YuanDepartment of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen, 518038, China.
Sixi LiuDepartment of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen, 518038, China. tiger647@sina.com.ORCID http://orcid.org/0000-0003-1674-2685
Feiqiu WenDepartment of Hematology and Oncology, Shenzhen Children's Hospital, Shenzhen, 518038, China. fwen62@163.com.ORCID http://orcid.org/0000-0001-5559-633X
Shenzhen Children's Hospital · CNJinan University · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm with increasing incidence worldwide. Growing evidence suggests that ubiquitin-specific proteases (USPs) play a role in cancer treatment. Dysregulation of miR-146a has been found in both adult and pediatric patients with acute leukemia. Knockdown of glutaminase-1 (GLS1) resulted in inhibition of tumor growth. However, the role of miR-146a-5p/USP6/GLS1 in leukemia and chemoresistance of leukemia cells remains to be elucidated. In the current study, USP6 level was increased in bone marrow aspiration specimens of patients with CML and associated with poor prognosis. USP6 was significantly upregulated in imatinib (IM)-resistant clinical samples compared with IM-sensitive samples. USP6 overexpression significantly inhibited IM-induced apoptosis of leukemia cells. Overexpressing USP6 significantly increased GLS1 ubiquitination to decrease GLS protein. A mechanism study indicated that USP6 regulation of IM resistance of CML cells was GLS1 dependent and regulated by miR-146a-5p. Administration of human umbilical cord mesenchymal stem cell (hucMSC) exosomes promoted IM-induced cell apoptosis through miR-145a-5p/USP6. Therefore, hucMSC exosomes promoted IM-induced apoptosis of K562-R cells by suppressing GLS1 ubiquitination to increase GLS protein via miR-146a-5p and its target GLS1. The findings highlight the importance of miR-146a-5p/USP6/GLS1 signaling in chemoresistance of leukemia and provide new insights into therapeutic strategies for chemoresistant leukemia.

Indexed as

ExosomesLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMicroRNAsAdultApoptosisChildDrug Resistance, NeoplasmGlutaminaseHumansImatinib MesylateK562 CellsUbiquitin ThiolesteraseGlutaminaseImatinib MesylateMicroRNAsUbiquitin ThiolesteraseUSP6 protein, human

Identifiers

PMID35091542
PMCPMC8799639
OpenAlexW4210358440

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.