Evidence map›Paper›PMID 29481642›Full record

ArticleNucleic acids research2018

LncRNA-OIS1 regulates DPP4 activation to modulate senescence induced by RAS.

Li Li, Pieter C van Breugel, Fabricio Loayza-Puch, Alejandro Pineiro Ugalde, Gozde Korkmaz, Naama Messika-Gold, Ruiqi Han, Rui Lopes, Eric P Barbera, Hans Teunissen and 10 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Liuwei Dihuang Prevents Human Umbilical Vein Endothelial Cells SenescenceCombinatorial chemistry & high throughput screening · 2026
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  7. Reliable Hallmarks and Biomarkers of Senescent Lymphocytes.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Emerging Role of Non-Coding RNAs in Senescence.Frontiers in cell and developmental biology · 2022
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. 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

20 authors at 6 institutions in 4 countries.

Li LiDivision of Oncogenomics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Pieter C van BreugelDivision of Oncogenomics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Fabricio Loayza-PuchDivision of Oncogenomics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Alejandro Pineiro UgaldeDivision of Oncogenomics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Gozde KorkmazDivision of Oncogenomics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Naama Messika-GoldDepartment of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, 69978, Tel Aviv University, Tel Aviv, Israel.
Ruiqi HanDivision of Oncogenomics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Rui LopesDivision of Oncogenomics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Eric P BarberaDivision of Molecular Genetics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Hans TeunissenDivision of Gene Regulation, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Elzo de WitDivision of Gene Regulation, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Ricardo J SoaresBioneer A/S, Kogle Allé 2, DK-2970 Hørsholm, Denmark.
Boye S NielsenBioneer A/S, Kogle Allé 2, DK-2970 Hørsholm, Denmark.
Kim HolmstrømBioneer A/S, Kogle Allé 2, DK-2970 Hørsholm, Denmark.
Dannys J Martínez-HerreraInstitute of Health Research of Navarra (IdiSNA), 31008 Pamplona, Spain.
Maite HuarteInstitute of Health Research of Navarra (IdiSNA), 31008 Pamplona, Spain.
Annita LouloupiDivision of Oncogenomics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Jarno DrostDivision of Oncogenomics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
Ran ElkonDepartment of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, 69978, Tel Aviv University, Tel Aviv, Israel.
Reuven AgamiDivision of Oncogenomics, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.
The Netherlands Cancer Institute · NLBioneer (Denmark) · DKNavarre Institute of Health Research · ESOncode Institute · NLTel Aviv University · ILErasmus University Rotterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncogene-induced senescence (OIS), provoked in response to oncogenic activation, is considered an important tumor suppressor mechanism. Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nt without a protein-coding capacity. Functional studies showed that deregulated lncRNA expression promote tumorigenesis and metastasis and that lncRNAs may exhibit tumor-suppressive and oncogenic function. Here, we first identified lncRNAs that were differentially expressed between senescent and non-senescent human fibroblast cells. Using RNA interference, we performed a loss-function screen targeting the differentially expressed lncRNAs, and identified lncRNA-OIS1 (lncRNA#32, AC008063.3 or ENSG00000233397) as a lncRNA required for OIS. Knockdown of lncRNA-OIS1 triggered bypass of senescence, higher proliferation rate, lower abundance of the cell-cycle inhibitor CDKN1A and high expression of cell-cycle-associated genes. Subcellular inspection of lncRNA-OIS1 indicated nuclear and cytosolic localization in both normal culture conditions as well as following oncogene induction. Interestingly, silencing lncRNA-OIS1 diminished the senescent-associated induction of a nearby gene (Dipeptidyl Peptidase 4, DPP4) with established role in tumor suppression. Intriguingly, similar to lncRNA-OIS1, silencing DPP4 caused senescence bypass, and ectopic expression of DPP4 in lncRNA-OIS1 knockdown cells restored the senescent phenotype. Thus, our data indicate that lncRNA-OIS1 links oncogenic induction and senescence with the activation of the tumor suppressor DPP4.

Indexed as

Cellular SenescenceDipeptidyl Peptidase 4Gene ExpressionGenes, rasGenomeHEK293 CellsHumansNeoplasmsRNA, Long NoncodingDipeptidyl Peptidase 4DPP4 protein, humanRNA, Long Noncoding

Identifiers

PMID29481642
PMCPMC5934637
OpenAlexW2790279177

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.