Evidence map›Paper›PMID 30521981›Full record

ArticleNeoplasia (New York, N.Y.)2019

Interferons Transcriptionally Up-Regulate MLKL Expression in Cancer Cells.

Anne-Kathrin Knuth, Stefanie Rösler, Barbara Schenk, Lisa Kowald, Sjoerd J L van Wijk, Simone Fulda

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Progress in study on the final executor of necroptosis MLKL and its inhibitors.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  19. T-box transcription factor 2 mediates antitumor immune response in cutaneous squamous cell carcinoma by regulating the expression of programmed death ligand 1.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2023
    Article
  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

6 authors at 2 institutions in 1 country.

Anne-Kathrin KnuthInstitute for Experimental Cancer Research in Pediatrics, Goethe-University, Frankfurt, Germany.
Stefanie RöslerInstitute for Experimental Cancer Research in Pediatrics, Goethe-University, Frankfurt, Germany.
Barbara SchenkInstitute for Experimental Cancer Research in Pediatrics, Goethe-University, Frankfurt, Germany.
Lisa KowaldInstitute for Experimental Cancer Research in Pediatrics, Goethe-University, Frankfurt, Germany.
Sjoerd J L van WijkInstitute for Experimental Cancer Research in Pediatrics, Goethe-University, Frankfurt, Germany.
Simone FuldaInstitute for Experimental Cancer Research in Pediatrics, Goethe-University, Frankfurt, Germany; German Cancer Consortium (DKTK), Partner Site, Frankfurt, Germany; German Cancer Research Center (DKFZ), Heidelberg, Germany. Electronic address: simone.fulda@kgu.de.
Frankfurt Cancer Institute · DEGoethe University Frankfurt · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferons (IFNs) are key players in the tumor immune response and act by inducing the expression of IFN-stimulated genes (ISGs). Here, we identify the mixed-lineage kinase domain-like pseudokinase (MLKL) as an ISG in various cancer cell lines. Both type I and type II IFNs increase the expression of MLKL indicating that MLKL up-regulation is a general feature of IFN signaling. IFNγ up-regulates mRNA as well as protein levels of MLKL demonstrating that IFNγ transcriptionally regulates MLKL. This notion is further supported by Actinomycin D chase experiments showing that IFNγ-stimulated up-regulation of MLKL is prevented in the presence of the transcriptional inhibitor Actinomycin D. Also, knockdown of the transcription factor IFN-regulatory factor 1 (IRF1) and signal transducer and activator of transcription (STAT) 1 as well as knockout of IRF1 significantly attenuate IFNγ-mediated induction of MLKL mRNA levels. Up-regulation of MLKL by IFNγ provides a valuable tool to sensitize cells towards necroptotic cell death and to overcome apoptosis resistance of cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticTranscriptional ActivationCaspasesCell Line, TumorHumansInterferon Regulatory Factor-1InterferonsNeoplasmsProtein KinasesRNA, MessengerSTAT1 Transcription FactorCaspasesInterferon Regulatory Factor-1InterferonsIRF1 protein, humanMLKL protein, humanProtein KinasesRNA, MessengerSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID30521981
PMCPMC6310689
OpenAlexW2902664945

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.