Evidence map›Paper›PMID 23475283›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2013

A DNA methylation signature associated with the epigenetic repression of glycine N-methyltransferase in human hepatocellular carcinoma.

Covadonga Huidobro, Estela G Toraño, Agustín F Fernández, Rocío G Urdinguio, Ramón M Rodríguez, Cecilia Ferrero, Pablo Martínez-Camblor, Loreto Boix, Jordi Bruix, Juan Luís García-Rodríguez and 4 more

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PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. DNA methylation markers in the detection of hepatocellular carcinoma.European journal of cancer (Oxford, England : 1990) · 2023
    Review
  5. Article
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  19. Modeling progressive non-alcoholic fatty liver disease in the laboratory mouse.Mammalian genome : official journal of the International Mammalian Genome Society · 2014
    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

14 authors at 5 institutions in 1 country.

Covadonga HuidobroCancer Epigenetics Laboratory, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), HUCA, Universidad de Oviedo, 33006 Oviedo, Spain.
Estela G Toraño
Agustín F Fernández
Rocío G Urdinguio
Ramón M Rodríguez
Cecilia Ferrero
Pablo Martínez-Camblor
Loreto Boix
Jordi Bruix
Juan Luís García-Rodríguez
Marta Varela-Rey
José María Mato
María Luz Martínez-Chantar
Mario F Fraga
Universidad de Oviedo · ESCIC bioGUNE · ESCentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas · ESCentro Nacional de Biotecnología · ESUniversitat de Barcelona · ES

Funding

Role of SAMe in Pathogenesis and Treatment of Non-Alcholic Fatty Liver DiseaseR01AT001576 · NCCIH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LU, SHELLY CHI-LOO · 2002 to 2018
$5.0M
REGULATION OF S-ADENOSYLMETHIONINE SYNTHETASE IN LIVERR01DK051719 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LU, SHELLY CHI-LOO · 1997 to 2014
$4.5M
Role of MAT and SAMe in Colon Cancer Pathogenesis and TreatmentR01AT004896 · NCCIH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LU, SHELLY CHI-LOO · 2008 to 2012
$2.0M
NCCIH NIH HHS R01AT004896NCCIH NIH HHS R01AT1576NIDDK NIH HHS R01DK051719
6 · The paper itself

Abstract

The basic mechanisms underlying promoter DNA hypermethylation in cancer are still largely unknown. It has been proposed that the levels of the methyl donor group in DNA methylation reactions, S-adenosylmethionine (SAMe), might be involved. SAMe levels depend on the glycine-N-methyltransferase (GNMT), a one-carbon group methyltransferase, which catalyzes the conversion of SAMe to S-adenosylhomocysteine in hepatic cells. GNMT has been proposed to display tumor suppressor activity and to be frequently repressed in hepatocellular carcinoma (HCC). In this study, we show that GNMT shows aberrant DNA hypermethylation in some HCC cell lines and primary tumors (20 %). GNMT hypermethylation could contribute to gene repression and its restoration in cell lines displaying hypermethylation-reduced tumor growth in vitro. In agreement, human primary tumors expressing GNMT were of smaller size than tumors showing GNMT hypermethylation. Genome-wide analyses of gene promoter methylation identified 277 genes whose aberrant methylation in HCC was associated with GNMT methylation/expression. The findings in this manuscript indicate that DNA hypermethylation plays an important role in the repression of GNMT in HCC and that loss of GNMT in human HCC could promote the establishment of aberrant DNA methylation patterns at specific gene promoters.

Indexed as

DNA MethylationCarcinoma, HepatocellularCell Line, TumorCell ProliferationCell SurvivalEpigenetic RepressionGlycine N-MethyltransferaseHistonesHumansLiver NeoplasmsRNA, MessengerS-AdenosylmethionineGlycine N-MethyltransferaseGNMT protein, humanHistonesRNA, MessengerS-Adenosylmethionine

Identifiers

PMID23475283
OpenAlexW2077216945

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.