Evidence map›Paper›PMID 19802007›Full record

ArticleOncogene2010

Cytokine expression and signaling in drug-induced cellular senescence.

Z Novakova, S Hubackova, M Kosar, L Janderova-Rossmeislova, J Dobrovolna, P Vasicova, M Vancurova, Z Horejsi, P Hozak, J Bartek and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
3.4field-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

65 citing papers in PubMed, 140 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Loss of H3K9 trimethylation leads to premature aging.bioRxiv : the preprint server for biology · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. ATOH8 binds SMAD3 to induce cellular senescence and prevent Ras-driven malignant transformation.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Acteoside ameliorates hepatic ischemia-reperfusion injuryInternational journal of biological sciences · 2023
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

5 more citing papers are in PubMed but not listed here.

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

11 authors at 4 institutions in 5 countries.

Z NovakovaDepartment of Genome Integrity, Institute of Molecular Genetics, v.v.i., Academy of Sciences of the Czech Republic, Prague, Czech Republic. hodny@img.cas.cz
S Hubackova
M Kosar
L Janderova-Rossmeislova
J Dobrovolna
P Vasicova
M Vancurova
Z Horejsi
P Hozak
J Bartek
Z Hodny
Czech Academy of Sciences · CZCzech Academy of Sciences, Institute of Molecular Genetics · CZCzech Academy of Sciences, Institute of Microbiology · CZHospital for Special Surgery · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence guards against cancer and modulates aging; however, the underlying mechanisms remain poorly understood. Here, we show that genotoxic drugs capable of inducing premature senescence in normal and cancer cells, such as 5-bromo-2'-deoxyuridine (BrdU), distamycin A (DMA), aphidicolin and hydroxyurea, persistently activate Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling and expression of interferon-stimulated genes (ISGs), such as MX1, OAS, ISG15, STAT1, PML, IRF1 and IRF7, in several human cancer cell lines. JAK1/STAT-activating ligands, interleukin 10 (IL10), IL20, IL24, interferon gamma (IFNgamma), IFNbeta and IL6, were also expressed by senescent cells, supporting autocrine/paracrine activation of JAK1/STAT. Furthermore, cytokine genes, including proinflammatory IL1, tumor necrosis factor and transforming growth factor families, were highly expressed. The strongest inducer of JAK/STAT signaling, cytokine production and senescence was BrdU combined with DMA. RNA interference-mediated knockdown of JAK1 abolished expression of ISGs, but not DNA damage signaling or senescence. Thus, although DNA damage signaling, p53 and RB activation, and the cytokine/chemokine secretory phenotype are apparently shared by all types of senescence, our data reveal so far unprecedented activation of the IFNbeta-STAT1-ISGs axis, and indicate a less prominent causative role of IL6-JAK/STAT signaling in genotoxic drug-induced senescence compared with reports on oncogene-induced or replicative senescence. These results highlight shared and unique features of drug-induced cellular senescence, and implicate induction of cancer secretory phenotype in chemotherapy.

Indexed as

Blotting, WesternBromodeoxyuridineCell Line, TumorCellular SenescenceCytokinesDistamycinsDrug SynergismHeLa CellsHumansInterferonsInterleukin-10Interleukin-24Interleukin-6Interleukin-8InterleukinsJanus Kinase 1BromodeoxyuridineCytokinesDistamycinsInterferonsInterleukin-10interleukin 20Interleukin-24Interleukin-6Interleukin-8InterleukinsJanus Kinase 1stallimycinSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID19802007
OpenAlexW2009703979

What OpenQuestion holds

Textmetadata
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.