Evidence map›Paper›PMID 28951459›Full record

ArticleCancer research2017

SMYD5 Controls Heterochromatin and Chromosome Integrity during Embryonic Stem Cell Differentiation.

Benjamin L Kidder, Runsheng He, Darawalee Wangsa, Hesed M Padilla-Nash, M Margarida Bernardo, Shijie Sheng, Thomas Ried, Keji Zhao

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  7. Article
  8. SMYD5 is a regulator of the mild hypothermia response.bioRxiv : the preprint server for biology · 2024
    Article
  9. Article
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  12. Article
  13. Review
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  18. Article
  19. The Prognostic Value and Mechanisms of TMEM16A in Human Cancer.Frontiers in molecular biosciences · 2021
    Review
  20. Review
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

8 authors at 1 institution in 1 country.

Benjamin L KidderDepartment of Oncology, Wayne State University School of Medicine, Detroit, Michigan. benjamin.kidder@wayne.edu zhaok@nhlbi.nih.gov.
Runsheng HeDepartment of Oncology, Wayne State University School of Medicine, Detroit, Michigan.
Darawalee WangsaCancer Genomics Section, National Cancer Institute, NIH, Bethesda, Maryland.
Hesed M Padilla-NashCancer Genomics Section, National Cancer Institute, NIH, Bethesda, Maryland.
M Margarida BernardoBarbara Ann Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan.
Shijie ShengBarbara Ann Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan.
Thomas RiedCancer Genomics Section, National Cancer Institute, NIH, Bethesda, Maryland.
Keji ZhaoSystems Biology Center, National Heart, Lung and Blood Institute, NIH, Bethesda, Maryland. benjamin.kidder@wayne.edu zhaok@nhlbi.nih.gov.
Wayne State University · US

Funding

Epigenetic Regulation of Hematopoietic Stem CellsZIAHL006031 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ZHAO, KEJI · 2009 to 2025
$16.6M
Regulation of chromatin and genome stability by the H4K20 methyltransferase SMYD5K22HL126842 · NHLBI · WAYNE STATE UNIVERSITY · PI KIDDER, BENJAMIN L · 2016 to 2018
$736k
NHLBI NIH HHS K22 HL126842
6 · The paper itself

Abstract

Epigenetic regulation of chromatin states is thought to control gene expression programs during lineage specification. However, the roles of repressive histone modifications, such as trimethylated histone lysine 20 (H4K20me3), in development and genome stability are largely unknown. Here, we show that depletion of SET and MYND domain-containing protein 5 (SMYD5), which mediates H4K20me3, leads to genome-wide decreases in H4K20me3 and H3K9me3 levels and derepression of endogenous LTR- and LINE-repetitive DNA elements during differentiation of mouse embryonic stem cells. SMYD5 depletion resulted in chromosomal aberrations and the formation of transformed cells that exhibited decreased H4K20me3 and H3K9me3 levels and an expression signature consistent with multiple human cancers. Moreover, dysregulated gene expression in SMYD5 cancer cells was associated with LTR and endogenous retrovirus elements and decreased H4K20me3. In addition, depletion of SMYD5 in human colon and lung cancer cells results in increased tumor growth and upregulation of genes overexpressed in colon and lung cancers, respectively. These findings implicate an important role for SMYD5 in maintaining chromosome integrity by regulating heterochromatin and repressing endogenous repetitive DNA elements during differentiation.

Indexed as

A549 CellsAnimalsBase SequenceCell DifferentiationCell Line, TumorChromosomesColonic NeoplasmsDNA Copy Number VariationsEmbryonic Stem CellsEpigenesis, GeneticHCT116 CellsHeterochromatinHistone CodeHistonesHumansLung NeoplasmsHeterochromatinHistonesMethyltransferasesRNA, Small InterferingSMYD5 protein, human

Identifiers

PMID28951459
PMCPMC5804482
OpenAlexW2758431699

What OpenQuestion holds

Textmetadata
LicenceTDM
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.