Evidence map›Paper›PMID 28860622›Full record

ArticleScientific reports2017

LSD1 modulates the non-canonical integrin β3 signaling pathway in non-small cell lung carcinoma cells.

So-Young Lim, Iris Macheleidt, Priya Dalvi, Stephan C Schäfer, Martin Kerick, Luka Ozretić, Sandra Ortiz-Cuaran, Julie George, Sabine Merkelbach-Bruse, Jürgen Wolf and 5 more

Erratum issuedAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Lung Cancer Therapy Targeting Histone Methylation: Opportunities and Challenges.Computational and structural biotechnology journal · 2018
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

So-Young LimInstitute of Pathology, University Hospital of Cologne, 50931, Cologne, Germany. so-young.lim@uk-koeln.de.
Iris MacheleidtInstitute of Pathology, University Hospital of Cologne, 50931, Cologne, Germany.
Priya DalviInstitute of Pathology, University Hospital of Cologne, 50931, Cologne, Germany.
Stephan C SchäferInstitute of Pathology, University Hospital of Cologne, 50931, Cologne, Germany.
Martin KerickFunctional Epigenomics, University of Cologne, 50931, Cologne, Germany.
Luka OzretićInstitute of Pathology, University Hospital of Cologne, 50931, Cologne, Germany.
Sandra Ortiz-CuaranCenter of Integrative Oncology, University Clinic of Cologne and Bonn, 50937, Cologne, Germany.
Julie GeorgeCenter of Integrative Oncology, University Clinic of Cologne and Bonn, 50937, Cologne, Germany.
Sabine Merkelbach-BruseInstitute of Pathology, University Hospital of Cologne, 50931, Cologne, Germany.
Jürgen WolfCenter of Integrative Oncology, University Clinic of Cologne and Bonn, 50937, Cologne, Germany.
Bernd TimmermannMax Planck Institute for Molecular Genetics, 14195, Berlin, Germany.
Roman K ThomasInstitute of Pathology, University Hospital of Cologne, 50931, Cologne, Germany.
Michal R SchweigerFunctional Epigenomics, University of Cologne, 50931, Cologne, Germany.
Reinhard BuettnerInstitute of Pathology, University Hospital of Cologne, 50931, Cologne, Germany.
Margarete OdenthalInstitute of Pathology, University Hospital of Cologne, 50931, Cologne, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epigenetic writer lysine-specific demethylase 1 (LSD1) is aberrantly upregulated in many cancer types and its overexpression correlates with poor survival and tumor progression. In this study, we analysed LSD1 function in non-small cell lung cancer adenocarcinomas. Expression profiling of 182 cases of lung adenocarcinoma proved a significant correlation of LSD1 overexpression with lung adenocarcinoma progression and metastasis. KRAS-mutated lung cancer cell clones were stably silenced for LSD1 expression. RNA-seq and comprehensive pathway analysis revealed, that genes related to a recently described non-canonical integrin β3 pathway, were significantly downregulated by LSD1 silencing. Hence, invasion and self-renewal capabilities were strongly decreased. Notably, this novel defined LSD1/integrin β3 axis, was also detected in human lung adenocarcinoma specimens. Furthermore, the linkage of LSD1 to an altered expression pattern of lung-lineage specific transcription factors and genes, which are involved in alveolar epithelial differentiation, was demonstrated. Thus, our findings point to a LSD1-integrin β3 axis, conferring attributes of invasiveness and tumor progression to lung adenocarcinoma.

Indexed as

AgedAged, 80 and overBiomarkersBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCells, CulturedFemaleGene ExpressionGene Knockdown TechniquesHistone DemethylasesHumansImmunohistochemistryIntegrin beta3Lung NeoplasmsBiomarkersBiomarkers, TumorHistone DemethylasesIntegrin beta3KDM1A protein, humanKRAS protein, humanNF-kappa BProto-Oncogene Proteins p21(ras)RNA, Messenger

Identifiers

PMID28860622
PMCPMC5578970

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.