Evidence map›Paper›PMID 32500672›Full record

ArticleThoracic cancer2020

Integrated analysis of miRNAs and DNA methylation identifies miR-132-3p as a tumor suppressor in lung adenocarcinoma.

Yun Su, Amol Shetty, Feng Jiang

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2020. 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
0.8field-weighted citation impact, top 34% 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, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Down-regulation ofInternational journal of molecular epidemiology and genetics · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. 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

3 authors at 2 institutions in 2 countries.

Yun SuDepartment of Surgery, Nanjing University of Chinese Medicine, Nanjing, China.
Amol ShettyInstitute for Genome Sciences, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Feng JiangDepartment of Pathology, University of Maryland School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0001-8510-3049
University of Maryland, Baltimore · USNanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAberrant miRNA expression and DNA methylation are two major epigenetic events in lung adenocarcinoma (LUAD). We conducted a combined analysis of the molecular changes in LUAD.

methodsWe analyzed differentially expressed miRNAs and methylated CpG loci in 489 LUAD tissues versus 49 normal lung tissues of the Cancer Genome Atlas (TCGA). The results were validated in cell lines and xenograft mouse models and additional pairs of 36 LUAD and 36 normal lung tissues.

resultsA total of 125 differentially expressed miRNAs and 145 differentially methylated CpG loci were identified in the LUAD versus normal lung tissues of TCGA data. Expression of the 22 miRNAs was inversely correlated with the 47 differentially methylated sites located in the miRNAs. Molecular and cellular function analysis showed that the abnormally methylated miRNAs were mainly involved in cell-to-cell signaling and interaction in airway cells. The DNA methylation status and altered expressions of miRNAs and their target genes were confirmed in 36 pairs of lung tumor and noncancerous lung tissues. Furthermore, aberrant miRNA expressions or DNA methylations alone could be involved in tumorigenesis of LUAD via different pathways. In addition, elevated miR-132-3p expression, reduced expression of its targeted gene (ZEB2), and decreased cell proliferation was observed in lung cancer cells treated with DNA methyltransferase inhibitor. Moreover, in vitro and in vivo analyses showed that miR-132-3p-3p downregulation via DNA methylation promoted tumorigenicity of lung cancer by directly regulating ZEB2.

conclusionsThe interaction between two epigenetic aberrations could have important functions in LUAD. miR-132-3p might act as a tumor suppressor in the tumorigenicity of LUAD. KEY POINTS: SIGNIFICANT FINDINGS OF THE STUDY: Systemically investigating relationship between aberrant miRNA expression and DNA methylation in lung cancer could improve understanding of lung tumorigenesis and develop diagnostic and therapeutic targets. WHAT THIS STUDY ADDS: Three forms of relationships between the two epigenetic changes are defined. miR-132-3p is further identified as a tumor suppressor in lung cancer.

Indexed as

DNA MethylationGenes, Tumor SuppressorAdenocarcinoma of LungAgedAnimalsHumansLung NeoplasmsMiceMicroRNAsMicroRNAsMIRN132 microRNA, humanDNA methylationepigeneticslung cancermicroRNA

Identifiers

PMID32500672
PMCPMC7396385
OpenAlexW3033560758

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.