Evidence map›Paper›PMID 37584287›Full record

ArticleHaematologica2024

miR-30e-5p regulates leukemia stem cell self-renewal through the Cyb561/ROS signaling pathway.

Yanwen Ge, Mei Hong, Yu Zhang, Jiachen Wang, Lei Li, Hongkai Zhu, Yue Sheng, Wen-Shu Wu, Zhonghui Zhang

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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Expression and clinical significance of cytochrome b561 in endometrial cancer.Journal of cancer research and clinical oncology · 2026
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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

9 authors at 5 institutions in 2 countries.

Yanwen GeSchool of Life Sciences, Shanghai University, Shanghai, 200444.
Mei HongSchool of Life Sciences, Shanghai University, Shanghai, 200444.
Yu ZhangSchool of Life Sciences, Shanghai University, Shanghai, 200444.
Jiachen WangSchool of Life Sciences, Shanghai University, Shanghai, 200444.
Lei LiDepartment of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022.
Hongkai ZhuDepartment of Hematology, The Second Xiangya Hospital, Central South University, Changsha, 410011.
Yue ShengDepartment of Hematology, The Second Xiangya Hospital, Central South University, Changsha, 410011.
Wen-Shu WuDivision of Hematology/Oncology, Department of Medicine and University of Illinois Cancer Center, the University of Illinois at Chicago, IL 60612. wuwenshu@uic.edu.
Zhonghui ZhangSchool of Life Sciences, Shanghai University, Shanghai, 200444, China; Shaoxing Institute of Technology, Shanghai University, Shaoxing, 312000. zhonghui@shu.edu.cn.
Shanghai University · CNCentral South University · CNHuazhong University of Science and Technology · CNSecond Xiangya Hospital of Central South University · CNUniversity of Illinois Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leukemia stem cells (LSC) represent a crucial and rare subset of cells present in acute myeloid leukemia (AML); they play a pivotal role in the initiation, maintenance, and relapse of this disease. Targeting LSC holds great promise for preventing AML relapse and improving long-term outcomes. However the precise molecular mechanisms governing LSC self-renewal are still poorly understood. Here, we present compelling evidence that the expression of miR-30e-5p, a potential tumor-suppressive microRNA, is significantly lower in AML samples than in healthy bone marrow samples. Forced expression of miR- 30e effectively inhibits leukemogenesis, impairs LSC self-renewal, and delays leukemia progression. Mechanistically, Cyb561 acts as a direct target of miR-30e-5p in LSC, and its deficiency restricts the self-renewal of LSC by activating reactive oxygen series signaling and markedly prolongs recipients' survival. Moreover, genetic or pharmacological overexpression of miR-30e-5p or knockdown of Cyb561 suppresses the growth of human AML cells. In conclusion, our findings establish the crucial role of the miR-30e-5p/Cyb561/ROS axis in finely regulating LSC self-renewal, highlighting Cyb561 as a potential therapeutic target for LSC-directed therapies.

Indexed as

Leukemia, Myeloid, AcuteMicroRNAsCell Line, TumorCell ProliferationCell Self RenewalHumansReactive Oxygen SpeciesRecurrenceSignal TransductionMicroRNAsReactive Oxygen Species

Identifiers

PMID37584287
PMCPMC10828755
OpenAlexW4385851682

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.