Evidence map›Paper›PMID 28440295›Full record

ArticleNature communications2017

KDM3 epigenetically controls tumorigenic potentials of human colorectal cancer stem cells through Wnt/β-catenin signalling.

Jiong Li, Bo Yu, Peng Deng, Yingduan Cheng, Yongxin Yu, Kareena Kevork, Sivakumar Ramadoss, Xiangming Ding, Xinmin Li, Cun-Yu Wang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
6.3field-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

95 citing papers in PubMed, 125 citations in OpenAlex.

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  18. Epigenetic regulation of cancer stemness.Signal transduction and targeted therapy · 2025
    Review
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  20. Review

35 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Jiong LiLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Broad Stem Cell Research Center, UCLA, Los Angeles, California 90095, USA.
Bo YuLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Broad Stem Cell Research Center, UCLA, Los Angeles, California 90095, USA.
Peng DengLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Broad Stem Cell Research Center, UCLA, Los Angeles, California 90095, USA.
Yingduan ChengLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Broad Stem Cell Research Center, UCLA, Los Angeles, California 90095, USA.
Yongxin YuLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Broad Stem Cell Research Center, UCLA, Los Angeles, California 90095, USA.
Kareena KevorkLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Broad Stem Cell Research Center, UCLA, Los Angeles, California 90095, USA.
Sivakumar RamadossLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Broad Stem Cell Research Center, UCLA, Los Angeles, California 90095, USA.
Xiangming DingDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California 90095, USA.
Xinmin LiDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine, UCLA, Los Angeles, California 90095, USA.
Cun-Yu WangLaboratory of Molecular Signaling, Division of Oral Biology and Medicine, School of Dentistry and Broad Stem Cell Research Center, UCLA, Los Angeles, California 90095, USA.
University of California, Los Angeles · US

Funding

Molecular and Genetic Determinants of Invasion in HNSCCR01DE015964 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, CUN-YU · 2004 to 2019
$6.6M
NIDCR NIH HHS R01 DE015964
6 · The paper itself

Abstract

Human colorectal cancer stem cells (CSCs) are tumour initiating cells that can self-renew and are highly tumorigenic and chemoresistant. While genetic mutations associated with human colorectal cancer development are well-known, little is known about how and whether epigenetic factors specifically contribute to the functional properties of human colorectal CSCs. Here we report that the KDM3 family of histone demethylases plays an important role in tumorigenic potential and survival of human colorectal CSCs by epigenetically activating Wnt target gene transcription. The depletion of KDM3 inhibits tumorigenic growth and chemoresistance of human colorectal CSCs. Mechanistically, KDM3 not only directly erases repressive H3K9me2 marks, but also helps to recruit histone methyltransferase MLL1 to promote H3K4 methylation, thereby promoting Wnt target gene transcription. Our results suggest that KDM3 is a critical epigenetic factor in Wnt signalling that orchestrates chromatin changes and transcription in human colorectal CSCs, identifying potential therapeutic targets for effective elimination of CSCs.

Indexed as

AnimalsCarcinogenesisCell Line, TumorCell ProliferationChromatinColorectal NeoplasmsDNA MethylationEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHistone-Lysine N-MethyltransferaseHistonesHumansJumonji Domain-Containing Histone DemethylasesMice, Inbred NODMice, NudeChromatinHistone-Lysine N-MethyltransferaseHistonesJMJD1C protein, humanJumonji Domain-Containing Histone DemethylasesKDM3A protein, humanKDM3B protein, humanKMT2A protein, humanMyeloid-Lymphoid Leukemia ProteinOxidoreductases, N-Demethylating

Identifiers

PMID28440295
PMCPMC5414094
OpenAlexW2608729572

What OpenQuestion holds

Textmetadata
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.