Evidence map›Paper›PMID 29568927›Full record

ArticleMolecular medicine reports2018

miR-185 and miR-29a are similarly expressed in the bronchoalveolar lavage cells in IPF and lung cancer but common targets DNMT1 and COL1A1 show disease specific patterns.

Eleni Bibaki, Eliza Tsitoura, Eirini Vasarmidi, George Margaritopoulos, Athina Trachalaki, Chara Koutoulaki, Theodora Georgopoulou, Demetrios A Spandidos, Nikos Tzanakis, Katerina M Antoniou

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Trial
  2. Reviewing the Regulators of COL1A1.International journal of molecular sciences · 2023
    Review
  3. Review
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  5. Article
  6. The role of exosomes from BALF in lung disease.Journal of cellular physiology · 2022
    Review
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  9. Article
  10. Review
  11. Article
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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

10 authors at 1 institution in 1 country.

Eleni BibakiLaboratory of Molecular and Cellular Pneumonology, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
Eliza TsitouraLaboratory of Molecular and Cellular Pneumonology, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
Eirini VasarmidiLaboratory of Molecular and Cellular Pneumonology, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
George MargaritopoulosLaboratory of Molecular and Cellular Pneumonology, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
Athina TrachalakiLaboratory of Molecular and Cellular Pneumonology, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
Chara KoutoulakiLaboratory of Molecular and Cellular Pneumonology, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
Theodora GeorgopoulouLaboratory of Molecular and Cellular Pneumonology, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
Demetrios A SpandidosLaboratory of Clinical Virology, Medical School, University of Crete, 71003 Heraklion, Crete, Greece.
Nikos TzanakisDepartment of Thoracic Medicine, Interstitial Lung Disease Unit, University Hospital, University of Crete, 71110 Heraklion, Crete, Greece.
Katerina M AntoniouLaboratory of Molecular and Cellular Pneumonology, Medical School, University of Crete, 71110 Heraklion, Crete, Greece.
University of Crete · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) and lung cancer (LC) constitute two progressively devastating lung diseases with common risk factors including aging and smoking. There is an increasing interest in the investigation of common pathogenic mechanisms between IPF and LC with therapeutic implications. Several oncomirs, microRNAs associated with malignancy, are also linked with IPF. miR‑29a and miR‑185 downregulation is probably involved both in carcinogenesis and fibrogenesis. We have previously observed miR‑29a and miR‑185 downregulation in IPF cells from bronchoalveolar lavage (BAL) and in this study we investigated their expression in LC BAL cells. Common targets of miR‑29a and miR‑185 such as DNA methyltransferase (DNMT)1, DNMT3b, COL1A1, AKT1 and AKT2 were measured. Potential correlations with pulmonary function tests, smoking status and endobronchial findings were investigated. Similar levels of miR‑29a and miR‑185 were detected in IPF and LC while their common targets AKT1 and DNMT3b were not found to differ, suggesting potential pathogenetic similarities at the level of key epigenetic regulators. By conrast, COL1A1 mRNA levels were increased in IPF suggesting a disease‑specific mRNA signature. Notably, DNMT1 was downregulated in the LC group and its expression was further reduced in the presence of increasing malignant burden as it was implied by the endobronchial findings.

Indexed as

Gene Expression RegulationAgedBronchoalveolar LavageBronchoalveolar Lavage FluidCells, CulturedCollagen Type ICollagen Type I, alpha 1 ChainDNA (Cytosine-5-)-Methyltransferase 1FemaleHumansIdiopathic Pulmonary FibrosisLung NeoplasmsMaleMicroRNAsMiddle AgedCollagen Type ICollagen Type I, alpha 1 ChainDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanMicroRNAsMIRN185 microRNA, humanMIRN29a microRNA, humanCOL1A1DNA methyltransferaseidiopathic pulmonary fibrosislung cancermicroRNAs

Identifiers

PMID29568927
PMCPMC5928671
OpenAlexW2793731902

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.