Evidence map›Paper›PMID 15007390›Full record

ArticleOncogene2004

Silencing of imprinted CDKN1C gene expression is associated with loss of CpG and histone H3 lysine 9 methylation at DMR-LIT1 in esophageal cancer.

Hidenobu Soejima, Tetsuji Nakagawachi, Wei Zhao, Ken Higashimoto, Takeshi Urano, Shiroh Matsukura, Yoshihiko Kitajima, Makoto Takeuchi, Masahiro Nakayama, Mitsuo Oshimura and 3 more

Abstract read
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Article in Oncogene, 2004. 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
2.0field-weighted citation impact, top 14% 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, 57 citations in OpenAlex.

  1. Review
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  17. Aberrant promoter methylation and expression of the imprinted PEG3 gene in glioma.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2009
    Article
  18. Article
  19. MicroRNA involvement in hepatocellular carcinoma.Journal of cellular and molecular medicine · 2008
    Review
  20. 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 5 institutions in 1 country.

Hidenobu SoejimaDepartment of Biomolecular Sciences, Division of Molecular Biology and Genetics, Saga Medical School, 5-1-1 Nabeshima, Saga 849-8501 Japan. soejimah@post.saga-med.ac.jp
Tetsuji Nakagawachi
Wei Zhao
Ken Higashimoto
Takeshi Urano
Shiroh Matsukura
Yoshihiko Kitajima
Makoto Takeuchi
Masahiro Nakayama
Mitsuo Oshimura
Kohji Miyazaki
Keiichiro Joh
Tsunehiro Mukai
Osaka Medical Center for Cancer and Cardiovascular Diseases · JPSaga Medical School Hospital · JPNagoya University · JPSaga University · JPTottori University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The putative tumor suppressor CDKN1C is an imprinted gene at 11p15.5, a well-known imprinted region often deleted in tumors. The absence of somatic mutations and the frequent diminished expression in tumors would suggest that CDKN1C expression is regulated epigenetically. It has been, however, controversial whether the diminution is caused by imprinting disruption of the CDKN1C/LIT1 domain or by promoter hypermethylation of CDKN1C itself. To clarify this, we investigated the CpG methylation index of the CDKN1C promoter and the differentially methylated region of the LIT1 CpG island (differentially methylated region (DMR)-LIT1), an imprinting control region of the domain, and CDKN1C expression in esophageal cancer cell lines. CDKN1C expression was diminished in 10 of 17 lines and statistically correlated with the loss of methylation at DMR-LIT1 in all but three. However, there was no statistical correlation between CDKN1C promoter MI and CDKN1C expression. Furthermore, loss of CpG methylation was associated with loss of histone H3 lysine 9 (H3K9) methylation at DMR-LIT1. Histone modifications at CDKN1C promoter were not correlated with CDKN1C expression. The data suggested that the diminished CDKN1C expression is associated with the loss of methylation of CpG and H3K9 at DMR-LIT1, not by its own promoter CpG methylation, and is involved in esophageal cancer, implying that DMR-LIT1 epigenetically regulates CDKN1C expression not through histone modifications at CDKN1C promoter, but through that of DMR-LIT1.

Indexed as

CpG IslandsDNA MethylationGene SilencingGenomic ImprintingCell Line, TumorChromosomes, Human, Pair 11Cyclin-Dependent Kinase Inhibitor p57Epigenesis, GeneticEsophageal NeoplasmsGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHistonesHumansMethylationNeoplasm ProteinsNuclear ProteinsCDKN1C protein, humanCyclin-Dependent Kinase Inhibitor p57HistonesKCNQ1OT1 RNANeoplasm ProteinsNuclear ProteinsRNA, Long NoncodingRNA, Untranslated

Identifiers

PMID15007390
OpenAlexW2025642178

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.