Evidence map›Paper›PMID 26644403›Full record

ArticleMolecular and cellular biology2016

Deregulated KLF4 Expression in Myeloid Leukemias Alters Cell Proliferation and Differentiation through MicroRNA and Gene Targets.

Valerie A Morris, Carrie L Cummings, Brendan Korb, Sean Boaglio, Vivian G Oehler

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 47 citations in OpenAlex.

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  15. Identification of Acute Myeloid Leukemia Bone Marrow Circulating MicroRNAs.International journal of molecular sciences · 2020
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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

5 authors at 2 institutions in 1 country.

Valerie A MorrisClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Carrie L CummingsClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Brendan KorbClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Sean BoaglioClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA.
Vivian G OehlerClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA Division of Hematology, Department of Medicine, University of Washington, Seattle, Washington, USA voehler@u.washington.edu.
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is characterized by increased proliferation and blocked differentiation of hematopoietic progenitors mediated, in part, by altered myeloid transcription factor expression. Decreased Krüppel-like factor 4 (KLF4) expression has been observed in AML, but how decreased KLF4 contributes to AML pathogenesis is largely unknown. We demonstrate decreased KLF4 expression in AML patient samples with various cytogenetic aberrations, confirm that KLF4 overexpression promotes myeloid differentiation and inhibits cell proliferation in AML cell lines, and identify new targets of KLF4. We have demonstrated that microRNA 150 (miR-150) expression is decreased in AML and that reintroducing miR-150 expression induces myeloid differentiation and inhibits proliferation of AML cells. We show that KLF family DNA binding sites are necessary for miR-150 promoter activity and that KLF2 or KLF4 overexpression induces miR-150 expression. miR-150 silencing, alone or in combination with silencing of CDKN1A, a well-described KLF4 target, did not fully reverse KLF4-mediated effects. Gene expression profiling and validation identified putative KLF4-regulated genes, including decreased MYC and downstream MYC-regulated gene expression in KLF4-overexpressing cells. Our findings indicate that decreased KLF4 expression mediates antileukemic effects through regulation of gene and microRNA networks, containing miR-150, CDKN1A, and MYC, and provide mechanistic support for therapeutic strategies increasing KLF4 expression.

Indexed as

Cell ProliferationGene Expression Regulation, LeukemicBase SequenceCell DifferentiationCell Line, TumorCyclin-Dependent Kinase Inhibitor p21HumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsLeukemia, MyeloidMicroRNAsMolecular Sequence DataPromoter Regions, GeneticCyclin-Dependent Kinase Inhibitor p21KLF2 protein, humanKLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAsMIR150, human

Identifiers

PMID26644403
PMCPMC4751692
OpenAlexW2201518863

What OpenQuestion holds

Textmetadata
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.