Evidence map›Paper›PMID 27977763›Full record

ArticlePloS one2016

TET1 Depletion Induces Aberrant CpG Methylation in Colorectal Cancer Cells.

Masahiro Kai, Takeshi Niinuma, Hiroshi Kitajima, Eiichiro Yamamoto, Taku Harada, Hironori Aoki, Reo Maruyama, Mutsumi Toyota, Yasushi Sasaki, Tamotsu Sugai and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
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  4. Plasmid-driven RNA interference in fish cell lines.In vitro cellular & developmental biology. Animal · 2022
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  8. Epigenetic silencing ofOncotarget · 2018
    Article
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

13 authors at 2 institutions in 1 country.

Masahiro KaiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takeshi NiinumaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiroshi KitajimaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Eiichiro YamamotoDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Taku HaradaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hironori AokiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Reo MaruyamaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Mutsumi ToyotaDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Yasushi SasakiMedical Genome Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Tamotsu SugaiDepartment of Molecular Diagnostic Pathology, Iwate Medical University, Morioka, Japan.
Takashi TokinoMedical Genome Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiroshi NakaseDepartment of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiromu SuzukiDepartment of Molecular Biology, Sapporo Medical University School of Medicine, Sapporo, Japan.ORCID http://orcid.org/0000-0001-9635-3238
Sapporo Medical University · JPIwate Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant DNA methylation is commonly observed in colorectal cancer (CRC), but the underlying mechanism is not fully understood. 5-hydroxymethylcytosine levels and TET1 expression are both reduced in CRC, while epigenetic silencing of TET1 is reportedly associated with the CpG island methylator phenotype. In the present study, we aimed to clarify the relationship between loss of TET1 and aberrant DNA methylation in CRC. Stable TET1 knockdown clones were established using Colo320DM cells, which express high levels of TET1, and HCT116 cells, which express TET1 at a level similar to that in normal colonic tissue. Infinium HumanMethylation450 BeadChip assays revealed increased levels of 5-methylcytosine at more than 10,000 CpG sites in TET1-depleted Colo320DM cells. Changes in DNA methylation were observed at various positions within the genome, including promoters, gene bodies and intergenic regions, and the altered methylation affected expression of a subset of genes. By contrast, TET1 knockdown did not significantly affect DNA methylation in HCT116 cells. However, TET1 depletion was associated with attenuated effects of 5-aza-2'-deoxycytidine on gene expression profiles in both cell lines. These results suggest that loss of TET1 may induce aberrant DNA methylation and may attenuate the effect of 5-aza-2'-deoxycytidine in CRC cells.

Indexed as

DNA MethylationAzacitidineCaco-2 CellsCell Line, TumorColorectal NeoplasmsCpG IslandsDecitabineDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGene SilencingHCT116 CellsHT29 CellsHumansMixed Function OxygenasesProto-Oncogene ProteinsRNA, Small InterferingAzacitidineDecitabineMixed Function OxygenasesProto-Oncogene ProteinsRNA, Small InterferingTET1 protein, human

Identifiers

PMID27977763
PMCPMC5158030
OpenAlexW2566261024

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.