Evidence map›Paper›PMID 10945503›Full record

ArticleBritish journal of cancer2000

Interferon-alpha2b reduces phosphorylation and activity of MEK and ERK through a Ras/Raf-independent mechanism.

F Romerio, A Riva, D Zella

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. EMT and Inflammation: Crossroads in HCC.Journal of gastrointestinal cancer · 2023
    Review
  4. Review
  5. Article
  6. OncoTargets and therapy · 2018
    Article
  7. Article
  8. Total chemical synthesis of human interferon alpha-2b via native chemical ligation.Journal of peptide science : an official publication of the European Peptide Society · 2015
    Article
  9. Review
  10. Review
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

3 authors at 2 institutions in 1 country.

F RomerioInstitute of Human Virology, University of Maryland Biotechnology Institute, Baltimore, Maryland 21201, USA.
A Riva
D Zella
Biotechnology Institute · USUniversity of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferon (IFN)-alpha affects the growth, differentiation and function of various cell types by transducing regulatory signals through the Janus tyrosine kinase/signal transducers of activation and transcription (Jak/STAT) pathway. The signalling pathways employing the mitogen-activated ERK-activating kinase (MEK) and the extracellular-regulated kinase (ERK) are critical in growth factors signalling. Engagement of the receptors, and subsequent stimulation of Ras and Raf, initiates a phosphorylative cascade leading to activation of several proteins among which MEK and ERK play a central role in routing signals critical in controlling cell development, activation and proliferation. We demonstrate here that 24-48 h following treatment of transformed T- and monocytoid cell lines with recombinant human IFN-alpha2b both the phosphorylation and activity of MEK1 and its substrates ERK1/2 were reduced. In contrast, the activities of the upstream molecules Ras and Raf-1 were not affected. No effect on MEK/ERK activity was observed upon short-term exposure (1-30 min) to IFN. The anti-proliferative effect of IFN-alpha was increased by the addition in the culture medium of a specific inhibitor of MEK, namely PD98059. In conclusion, our results indicate that IFN-alpha regulates the activity of the MEK/ERK pathway and consequently modulates cellular proliferation through a Ras/Raf-independent mechanism. Targeting the MEK/ERK pathway may strengthen the IFN-mediated anti-cancer effect.

Indexed as

Antineoplastic AgentsCell DivisionCell Line, TransformedDepression, ChemicalEnzyme InhibitorsFlavonoidsHumansInterferon-alphaInterferon alpha-2Jurkat CellsMAP Kinase Kinase 1MAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein Kinases2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneAntineoplastic AgentsEnzyme InhibitorsFlavonoidsHRAS protein, humanInterferon-alphaInterferon alpha-2MAP2K1 protein, humanMAP Kinase Kinase 1Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase KinasesMitogen-Activated Protein KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-rafProto-Oncogene Proteins p21(ras)Recombinant Proteins

Identifiers

PMID10945503
PMCPMC2374650
OpenAlexW1976722821

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.