Evidence map›Paper›PMID 32066721›Full record

ArticleNature communications2020

FOXM1 regulates leukemia stem cell quiescence and survival in MLL-rearranged AML.

Yue Sheng, Chunjie Yu, Yin Liu, Chao Hu, Rui Ma, Xinyan Lu, Peng Ji, Jianjun Chen, Benjamin Mizukawa, Yong Huang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 84 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 6 institutions in 1 country.

Yue ShengDivision of Hematology/Oncology, UF Health Cancer Center, University of Florida, Gainesville, FL, USA.
Chunjie YuDivision of Hematology/Oncology, UF Health Cancer Center, University of Florida, Gainesville, FL, USA.
Yin LiuDivision of Hematology/Oncology, UF Health Cancer Center, University of Florida, Gainesville, FL, USA.
Chao HuDepartment of Medicine, University of Illinois at Chicago, Chicago, IL, USA.
Rui MaInstitute for Tuberculosis Research, University of Illinois at Chicago, Chicago, IL, USA.
Xinyan LuDepartment of Pathology, Feinberg School of Medicine, Northwestern University, IL, USA.
Peng JiDepartment of Pathology, Feinberg School of Medicine, Northwestern University, IL, USA.ORCID http://orcid.org/0000-0002-8849-3625
Jianjun ChenDepartment of System Biology, City of Hope, CA, USA.ORCID http://orcid.org/0000-0003-3749-2902
Benjamin MizukawaCancer & Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.ORCID http://orcid.org/0000-0002-3312-2982
Yong HuangDepartment of Medicine, University of Virginia, Charlottestville, VA, USA.
Jonathan D LichtDivision of Hematology/Oncology, UF Health Cancer Center, University of Florida, Gainesville, FL, USA.ORCID http://orcid.org/0000-0002-3942-1369
Zhijian QianDivision of Hematology/Oncology, UF Health Cancer Center, University of Florida, Gainesville, FL, USA. zhijian.qian@medicine.ufl.edu.
University of Florida Health · USNorthwestern University · USUniversity of Illinois Chicago · USCincinnati Children's Hospital Medical Center · USCity of Hope · USUniversity of Virginia · US

Funding

The role of EVI1-induced hypermethylation in leukemogenesis.R01HL131444 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI QIAN, ZHIJIAN · 2016 to 2019
$1.6M
The molecular mechanism of clonal dominance in 5q(del) MDSR01DK107615 · NIDDK · UNIVERSITY OF ILLINOIS AT CHICAGO · PI QIAN, ZHIJIAN · 2016 to 2019
$1.4M
NHLBI NIH HHS R01 HL131444NIDDK NIH HHS R01 DK107615
6 · The paper itself

Abstract

FOXM1, a known transcription factor, promotes cell proliferation in a variety of cancer cells. Here we show that Foxm1 is required for survival, quiescence and self-renewal of MLL-AF9 (MA9)-transformed leukemia stem cells (LSCs) in vivo. Mechanistically, Foxm1 upregulation activates the Wnt/β-catenin signaling pathways by directly binding to β-catenin and stabilizing β-catenin protein through inhibiting its degradation, thereby preserving LSC quiescence, and promoting LSC self-renewal in MLL-rearranged AML. More importantly, inhibition of FOXM1 markedly suppresses leukemogenic potential and induces apoptosis of primary LSCs from MLL-rearranged AML patients in vitro and in vivo in xenograft mice. Thus, our study shows a critical role and mechanisms of Foxm1 in MA9-LSCs, and indicates that FOXM1 is a potential therapeutic target for selectively eliminating LSCs in MLL-rearranged AML.

Indexed as

Gene Expression Regulation, LeukemicAnimalsApoptosisCell Line, TumorCell ProliferationForkhead Box Protein M1Gene RearrangementHumansLeukemia, Myeloid, AcuteMiceMice, KnockoutMyeloid-Lymphoid Leukemia ProteinNeoplastic Stem CellsOncogene Proteins, FusionPrimary Cell CultureRNA-SeqForkhead Box Protein M1FOXM1 protein, humanFoxm1 protein, mouseMLL-AF9 fusion protein, humanMLL-AF9 fusion protein, mouseMyeloid-Lymphoid Leukemia ProteinOncogene Proteins, Fusion

Identifiers

PMID32066721
PMCPMC7026046
OpenAlexW3006415577

What OpenQuestion holds

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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.