Evidence map›Paper›PMID 22249264›Full record

ArticleOncogene2012

MicroRNA-29b is involved in the Src-ID1 signaling pathway and is dysregulated in human lung adenocarcinoma.

S I Rothschild, M P Tschan, E A Federzoni, R Jaggi, M F Fey, M Gugger, O Gautschi

Abstract read
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In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Review
  3. MiRNAs in Lung Adenocarcinoma: Role, Diagnosis, Prognosis, and Therapy.International journal of molecular sciences · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Cell Behavior of Non-Small Cell Lung Cancer Is at EGFR and MicroRNAs Hands.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Baicalein Inhibits Orthotopic Human Non-Small Cell Lung Cancer Xenografts via Src/Id1 Pathway.Evidence-based complementary and alternative medicine : eCAM · 2019
    Article
  15. Article
  16. miR-29 Family Inhibits Resistance to Methotrexate and Promotes Cell Apoptosis by Targeting COL3A1 and MCL1 in Osteosarcoma.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  17. Article
  18. Article
  19. Review
  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

7 authors at 3 institutions in 1 country.

S I RothschildDepartment of Clinical Research, University of Bern, and Department of Medical Oncology, Inselspital, Bern University Hospital, Bern, Switzerland.
M P Tschan
E A Federzoni
R Jaggi
M F Fey
M Gugger
O Gautschi
University of Bern · CHUniversity Hospital of Basel · CHUniversity Hospital of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The c-Src kinase regulates cancer cell invasion through inhibitor of DNA binding/differentiation 1 (ID1). Src and ID1 are frequently overexpressed in human lung adenocarcinoma. The current study aimed at identifying microRNAs (miRNAs) involved in the Src-ID1 signaling in lung cancer. Incubation of lung cancer cells with the Src inhibitor saracatinib led to the upregulation of several miRNAs including miR-29b, which was the most highly upregulated miRNA with predicted binding to the ID1 3'-untranslated region (UTR). Luciferase reporter assays confirmed direct binding of miR-29b to the ID1 3'-UTR. Expression of miR-29b suppressed ID1 levels and significantly reduced migration and invasion. Expression of antisense-miR-29b (anti-miR-29b), on the other hand, enhanced ID1 mRNA and protein levels, and significantly increased lung cancer cell migration and invasion, a hallmark of the Src-ID1 pathway. The ectopic expression of ID1 in miR-29b-overexpressing cells was able to rescue the migratory potential of these cells. Both, anti-miR-29b and ID1 overexpression diminished the effects of the Src inhibitors saracatinib and dasatinib on migration and invasion. Saracatinib and dasatinib decreased c-Myc transcriptional repression on miR-29b and led to increased ID1 protein levels, whereas forced expression of c-Myc repressed miR-29b and induced ID1. In agreement, we showed direct recruitment of c-Myc to the miR-29b promoter. miR-29b was significantly downregulated in primary lung adenocarcinoma samples compared with matched alveolar lung tissue, and miR-29b expression was a significant prognostic factor for patient outcome. These results suggest that miR-29b is involved in the Src-ID1 signaling pathway, is dysregulated in lung adenocarcinoma and is a potential predictive marker for Src kinase inhibitors.

Indexed as

Gene Expression Regulation, NeoplasticSignal Transduction3' Untranslated RegionsAdenocarcinomaAdenocarcinoma of LungCell Line, TumorCell MovementGene Expression ProfilingGenes, mycHumansInhibitor of Differentiation Protein 1Lung NeoplasmsMicroRNAsPrognosisProtein Kinase InhibitorsRNA Interference3' Untranslated RegionsInhibitor of Differentiation Protein 1MicroRNAsMIRN29a microRNA, humanProtein Kinase InhibitorsRNA, Small Interferingsrc-Family Kinases

Identifiers

PMID22249264
OpenAlexW2076110053

What OpenQuestion holds

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Registered trials

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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.