Cited by 649Macrophage Migration Inhibitory FactorCancer-related Molecular PathwaysMechanisms of cancer metastasis

A Proinflammatory Cytokine Inhibits P53 Tumor Suppressor Activity

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Hudson, James D., Shoaibi, Mahmood A., Maestro, Roberta, Carnero, Amancio, Hannon, Gregory J., Beach, David H.·1999·The Journal of Experimental Medicine

Abstract

p53 has a key role in the negative regulation of cell proliferation, in the maintenance of genomic stability, and in the suppression of transformation and tumorigenesis. To identify novel regulators of p53, we undertook two functional screens to isolate genes which bypassed either p53-mediated growth arrest or apoptosis. In both screens, we isolated cDNAs encoding macrophage migration inhibitory factor (MIF), a cytokine that was shown previously to exert both local and systemic proinflammatory activities. Treatment with MIF overcame p53 activity in three different biological assays, and suppressed its activity as a transcriptional activator. The observation that a proinflammatory cytokine, MIF, is capable of functionally inactivating a tumor suppressor, p53, may provide a link between inflammation and tumorigenesis.

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Crossref · 10.1084/jem.190.10.1375

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  • MIF is a potent cytokine that overcomes p53 function by suppressing its transcriptional activity.

    “MIF is a potent cytokine that overcomes p53 function by suppressing its transcriptional activity33.”

    From Inflammation and cancer (2002) · cites this paper as [33]

  • Tetracycline-regulated expression of wild-type p53 (GFP tagged) in the TGP53-4 mouse cell line caused a significant decline in endogenous PGM activity.

    “tetracycline regulated expression of wild-type p53 (GFP tagged) in the TGP53-4 mouse cell line (27) caused a significant decline in endogenous PGM activity (Fig. 5B).”

    From Glycolytic Enzymes Can Modulate Cellular Life Span (2005) · cites this paper as [27]

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Research works printed but not linked: 1

  1. Christen S. Hagen T.M. Shigenaga M.K. Ames B.N. Chronic infection and inflammation lead to cancer Parsonnet J. Horning S. Microbes and MalignancyInfection as a Cause of Cancer 1999 Oxford University Press Oxford

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Authors
Hudson, J. D., Shoaibi, M. A., Maestro, R., Carnero, A., Hannon, G. J., & Beach, D. H.
Affiliations
  • aUnit of Cancer Biology, Institute of Child Health, London WC1N 1EH, United Kingdom
  • Centro di Riferimento Oncologico (IT)
  • Cold Spring Harbor Laboratory (US)
Venue
The Journal of Experimental Medicine
Published
1999-11-15
Volume
190
Issue
10
Pages
1375-1382
ISSN
  • 0022-1007 (ISSN-L)
  • 1540-9538
OpenAlex
W2110929110
Cited by
649
References
48
Citations by year
2026: 8 · 2025: 12 · 2024: 14 · 2023: 10 · 2022: 12 · 2021: 18 · 2020: 25 · 2019: 17 · 2018: 14 · 2017: 14 · 2016: 27 · 2015: 24 · 2014: 25 · 2013: 25 · 2012: 38
FWCI
9.23
Type
journal article
Language
en
Open access
Locations
  • The Journal of Experimental Medicine (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
  • Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
  • DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, other-oa)
Funders
  • University College London
  • Associazione Italiana per la Ricerca sul Cancro
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Macrophage Migration Inhibitory Factor
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
Keywords
p53, macrophage migration inhibitory factor, inflammatory cytokines, tumor suppressor inactivation, inflammation and tumorigenesis, p53 transcriptional activation, apoptosis, cell proliferation, genome stability
MeSH terms
Animals, Cell Line, Chronic Disease, Fibroblasts, Inflammation, Macrophage Migration-Inhibitory Factors, Neoplasms, Nitric Oxide, Transcriptional Activation, Tumor Suppressor Protein p53, Apoptosis, Mice, Rats

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