Evidence map›Paper›PMID 25063738›Full record

ArticleCancer letters2014

Epigenetic silencing of microRNA-373 to epithelial-mesenchymal transition in non-small cell lung cancer through IRAK2 and LAMP1 axes.

Hyang Sook Seol, Yoshimitsu Akiyama, Shu Shimada, Hee Jin Lee, Tae Im Kim, Sung Min Chun, Shree Ram Singh, Se Jin Jang

Open access · greenAbstract read
In one paragraph

Article in Cancer letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 65 citations in OpenAlex.

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  13. Targeting Epigenetics in Lung Cancer.Cold Spring Harbor perspectives in medicine · 2021
    Review
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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 2 institutions in 2 countries.

Hyang Sook SeolDepartment of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea; Asan Center for Cancer Genome Discovery, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea.
Yoshimitsu AkiyamaDepartment of Molecular Oncology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Shu ShimadaDepartment of Molecular Oncology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo 113-8519, Japan.
Hee Jin LeeDepartment of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea.
Tae Im KimAsan Center for Cancer Genome Discovery, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea.
Sung Min ChunDepartment of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea; Asan Center for Cancer Genome Discovery, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea.
Shree Ram SinghBasic Research Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA. Electronic address: singhshr@mail.nih.gov.
Se Jin JangDepartment of Pathology, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea; Asan Center for Cancer Genome Discovery, University of Ulsan College of Medicine, Asan Medical Center, Seoul 138-736, South Korea. Electronic address: jangsejin@amc.seoul.kr.
Tokyo Medical and Dental University · JPUlsan College · KR

Funding

Molecular Genetic Study of Stem Cells, Cancer Stem Cells, and Stem Cell AgingZ01BC010738 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HOU, XIANYU S · 2006 to 2008
$2.7M
Intramural NIH HHS Z01 BC010738Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

The role of microRNAs (miRNAs) in carcinogenesis as tumor suppressors or oncogenes has been widely reported. Epigenetic change is one of the mechanisms of transcriptional silencing of miRNAs in cancer. To identify lung cancer-related miRNAs that are mediated by histone modification, we conducted microarray analysis in the Calu-6 non-small cell lung cancer (NSCLC) cell line after treatment with suberoylanilide hydroxamic acid (SAHA), a histone deacetylase (HDAC) inhibitor. The expression level of miR-373 was enhanced by SAHA treatment in this cell line by microarray and the following quantitative RT-PCR analyses. Treatment with another HDAC inhibitor, Trichostatin A, restored the levels of miR-373 expression in A549 and Calu-6 cells, while demethylation drug treatment did not. Importantly, miR-373 was found to be down-regulated in NSCLC tissues and cell lines. Transfection of miR-373 into A549 and Calu-6 cells attenuated cell proliferation, migration, and invasion and reduced the expression of mesenchymal markers. Additional microarray analysis of miR-373-transfected cells and computational predictions identified IRAK2 and LAMP1 as targets of miR-373. Knockdown of these two genes showed similar biological effects to those of miR-373 overexpression. In clinical samples, overexpression of IRAK2 correlated with decreased disease-free survival of patients with non-adenocarcinoma. In conclusion, we found that miR-373 is silenced by histone modification in lung cancer cells and identified its function as a tumor suppressor and negative regulator of the mesenchymal phenotype through downstream IRAK2 and LAMP1 target genes.

Indexed as

Epigenesis, GeneticCarcinoma, Non-Small-Cell LungCell Line, TumorDisease-Free SurvivalEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHistonesHumansInterleukin-1 Receptor-Associated KinasesKaplan-Meier EstimateLung NeoplasmsLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsMaleMicroRNAsHistonesInterleukin-1 Receptor-Associated KinasesLAMP1 protein, humanLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsMicroRNAsMIRN373 microRNA, humanHistone deacetylaseIRAK2LAMP1microRNA-373Non-small cell lung cancerTumor suppressor

Identifiers

PMID25063738
PMCPMC7707239
OpenAlexW2152207829

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.