Evidence map›Paper›PMID 25288800›Full record

ArticleThe Journal of biological chemistry2014

Kruppel-like factor-9 (KLF9) inhibits glioblastoma stemness through global transcription repression and integrin α6 inhibition.

Mingyao Ying, Jessica Tilghman, Yingying Wei, Hugo Guerrero-Cazares, Alfredo Quinones-Hinojosa, Hongkai Ji, John Laterra

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

47 citing papers in PubMed, 77 citations in OpenAlex.

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  7. Integrins in cancer stem cells.Frontiers in cell and developmental biology · 2024
    Review
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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

7 authors at 3 institutions in 2 countries.

Mingyao YingFrom the Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, Maryland 21205, Departments of Neurology.
Jessica TilghmanFrom the Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, Maryland 21205, Neuroscience.
Yingying WeiDepartment of Statistics, Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, China.
Hugo Guerrero-CazaresNeurosurgery, The Johns Hopkins School of Medicine, Baltimore, Maryland 21205.
Alfredo Quinones-HinojosaNeuroscience, Neurosurgery, The Johns Hopkins School of Medicine, Baltimore, Maryland 21205, Oncology, and.
Hongkai JiDepartment of Biostatistics, The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, 21205, and.
John LaterraFrom the Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, Maryland 21205, Departments of Neurology, Neuroscience, Oncology, and laterra@kennedykrieger.org.
Johns Hopkins University · USChinese University of Hong Kong · CNKennedy Krieger Institute · US

Funding

Role of NKCC1 on Brain Tumor Stem Cell Migration After EGF and Slit-2 StimulationR01NS070024 · NINDS · JOHNS HOPKINS UNIVERSITY · PI QUINONES-HINOJOSA, ALFREDO · 2010 to 2014
$2.4M
Brain Cancer Stem Cell Reprogramming by c-MetR01NS073611 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J · 2012 to 2016
$1.8M
Suppression of Glioblastoma Stem Cells by Kruppel-Like Factor 9R01NS076759 · NINDS · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI LATERRA, JOHN J · 2011 to 2015
$1.6M
Statistical and Computational Tools for Next-generation ChIP-seq ApplicationsR01HG006841 · NHGRI · JOHNS HOPKINS UNIVERSITY · PI JI, HONGKAI · 2012 to 2014
$951k
NHGRI NIH HHS R01 HG006841NHGRI NIH HHS R01HG006841NINDS NIH HHS R01 5R01NS070024NINDS NIH HHS R01 NS070024NINDS NIH HHS R01 NS073611NINDS NIH HHS R01NS073611NINDS NIH HHS R01 NS076759NINDS NIH HHS R01NS076759
6 · The paper itself

Abstract

It is increasingly important to understand the molecular basis for the plasticity of neoplastic cells and their capacity to transition between differentiated and stemlike phenotypes. Kruppel-like factor-9 (KLF9), a member of the large KLF transcription factor family, has emerged as a regulator of oncogenesis, cell differentiation, and neural development; however, the molecular basis for the diverse contextual functions of KLF9 remains unclear. This study focused on the functions of KLF9 in human glioblastoma stemlike cells. We established for the first time a genome-wide map of KLF9-regulated targets in human glioblastoma stemlike cells and show that KLF9 functions as a transcriptional repressor and thereby regulates multiple signaling pathways involved in oncogenesis and stem cell regulation. A detailed analysis of one such pathway, integrin signaling, showed that the capacity of KLF9 to inhibit glioblastoma cell stemness and tumorigenicity requires ITGA6 repression. These findings enhance our understanding of the transcriptional networks underlying cancer cell stemness and differentiation and identify KLF9-regulated molecular targets applicable to cancer therapeutics.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntibiotics, AntineoplasticBlotting, WesternCell DifferentiationCell Line, TumorDoxorubicinGlioblastomaHumansIntegrin alpha6Kruppel-Like Transcription FactorsMice, SCIDPromoter Regions, GeneticProtein BindingReverse Transcriptase Polymerase Chain ReactionTransplantation, HeterologousAntibiotics, AntineoplasticDoxorubicinIntegrin alpha6KLF9 protein, humanKruppel-Like Transcription FactorsCancer Stem CellsChIP-Sequencing (ChIP-Seq)GlioblastomaKruppel-like Factor (KLF)Transcription Repressor

Identifiers

PMID25288800
PMCPMC4239625
OpenAlexW2331704657

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.