Evidence map›Paper›PMID 26256448›Full record

ArticleCancer medicine2015

Histone methylation-mediated silencing of miR-139 enhances invasion of non-small-cell lung cancer.

Kousuke Watanabe, Yosuke Amano, Rie Ishikawa, Mitsuhiro Sunohara, Hidenori Kage, Junji Ichinose, Atsushi Sano, Jun Nakajima, Masashi Fukayama, Yutaka Yatomi and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Cells · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  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 1 institution in 1 country.

Kousuke WatanabeDepartment of Respiratory Medicine, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Yosuke AmanoDepartment of Respiratory Medicine, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Rie IshikawaDepartment of Respiratory Medicine, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Mitsuhiro SunoharaDepartment of Respiratory Medicine, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Hidenori KageDepartment of Respiratory Medicine, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Junji IchinoseDepartment of Cardiothoracic Surgery, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Atsushi SanoDepartment of Cardiothoracic Surgery, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Jun NakajimaDepartment of Cardiothoracic Surgery, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Masashi FukayamaDepartment of Pathology, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Yutaka YatomiDepartment of Clinical Laboratory, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Takahide NagaseDepartment of Respiratory Medicine, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Nobuya OhishiDepartment of Respiratory Medicine, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
Daiya TakaiDepartment of Clinical Laboratory, The University of Tokyo Hospital, Hongo, Bunkyo-ku, Tokyo, Japan.
University of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNA expression is frequently altered in human cancers, and some microRNAs act as oncogenes or tumor suppressors. MiR-139-5p (denoted thereafter as miR-139) has recently been reported to function as a tumor suppressor in several types of human cancer (hepatocellular carcinoma, colorectal cancer, breast cancer, and gastric cancer), but its function in non-small-cell lung cancer (NSCLC) and the mechanism of its suppression have not been studied in detail. MiR-139 was suppressed frequently in primary NSCLCs. MiR-139 is located within the intron of PDE2A and its expression was significantly correlated with the expression of PDE2A. A chromatin immunoprecipitation assay revealed that miR-139 was epigenetically silenced by histone H3 lysine 27 trimethylation (H3K27me3) of its host gene PDE2A and this process was independent of promoter DNA methylation. Pharmacological inhibition of both histone methylation and deacetylation-induced miR-139 with its host gene PDE2A. Ectopic expression of miR-139 in lung cancer cell lines did not affect the proliferation nor the migration but significantly suppressed the invasion through the extracellular matrix. In primary NSCLCs, decreased expression of miR-139 was significantly associated with distant lymph node metastasis and histological invasiveness (lymphatic invasion and vascular invasion) on both univariate and multivariate analyses. Collectively, these results suggest that H3K27me3-mediated silencing of miR-139 enhances an invasive and metastatic phenotype of NSCLC.

Indexed as

Gene SilencingCarcinoma, Non-Small-Cell LungCell Line, TumorCyclic Nucleotide Phosphodiesterases, Type 2DNA MethylationEctopic Gene ExpressionFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHistonesHumansLung NeoplasmsLymphatic MetastasisMaleMicroRNAsNeoplasm InvasivenessCyclic Nucleotide Phosphodiesterases, Type 2HistonesMicroRNAsMIRN139 microRNA, humanPDE2A protein, humanEpigenetic repressionhistoneslung neoplasmsmicroRNAsneoplasm metastasis

Identifiers

PMID26256448
PMCPMC4618627
OpenAlexW1619927893

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.