Evidence map›Paper›PMID 18684922›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Cooperative regulation of non-small cell lung carcinoma angiogenic potential by macrophage migration inhibitory factor and its homolog, D-dopachrome tautomerase.

Arlixer M Coleman, Beatriz E Rendon, Ming Zhao, Ming-Wei Qian, Richard Bucala, Dan Xin, Robert A Mitchell

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

62 citing papers in PubMed, 97 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. MIF contribution to progressive brain diseases.Journal of neuroinflammation · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Recent Advances in PROTACs for Drug Targeted Protein Research.International journal of molecular sciences · 2022
    Review
  13. Review
  14. Review
  15. Article
  16. Thieno[2,3-Journal of medicinal chemistry · 2022
    Article
  17. Review
  18. Article
  19. Review
  20. Article

2 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

7 authors at 4 institutions in 4 countries.

Arlixer M ColemanMicrobiology and Immunology Program, School of Medicine, University of Louisville, Louisville, KY 40202, USA.
Beatriz E Rendon
Ming Zhao
Ming-Wei Qian
Richard Bucala
Dan Xin
Robert A Mitchell
University of Louisville · USCentre of Excellence in Molecular Biology · PKCzech Academy of Sciences, Institute of Microbiology · CZYale University · US

Funding

MIF AND THE HOST RESPONSE TO INFECTIONR01AI042310 · NIAID · YALE UNIVERSITY · PI BUCALA, RICHARD J · 1998 to 2013
$4.3M
Role of MIF in Rb inactivation and TumorigenesisR01CA102285 · NCI · UNIVERSITY OF LOUISVILLE · PI MITCHELL, ROBERT A · 2004 to 2009
$1.4M
MIF and Host Response to InfectionR56AI042310 · NIAID · YALE UNIVERSITY · PI BUCALA, RICHARD J · 2014 to 2014
$426k
NCI NIH HHS CA102285NCI NIH HHS CA102285-SNCI NIH HHS R01 CA102285NIAID NIH HHS AI042310NIAID NIH HHS R01 AI042310NIAID NIH HHS R56 AI042310
6 · The paper itself

Abstract

Tumor-derived growth factors and cytokines stimulate neoangiogenesis from surrounding capillaries to support tumor growth. Recent studies have revealed that macrophage migration inhibitory factor (MIF) expression is increased in lung cancer, particularly non-small cell lung carcinomas (NSCLC). Because MIF has important autocrine effects on normal and transformed cells, we investigated whether autocrine MIF and its only known family member, D-dopachrome tautomerase (D-DT), promote the expression of proangiogenic factors CXCL8 and vascular endothelial growth factor in NSCLC cells. Our results demonstrate that the expression of CXCL8 and vascular endothelial growth factor are strongly reliant upon both the individual and cooperative activities of the two family members. CXCL8 transcriptional regulation by MIF and D-DT appears to involve a signaling pathway that includes the activation of JNK, c-jun phosphorylation, and subsequent AP-1 transcription factor activity. Importantly, HUVEC migration and tube formation induced by supernatants from lung adenocarcinoma cells lacking either or both MIF and D-DT are substantially reduced when compared with normal supernatants. Finally, we demonstrate that the cognate MIF receptor, CD74, is necessary for both MIF- and D-DT-induced JNK activation and CXCL8 expression, suggesting its potential involvement in angiogenic growth factor expression. This is the first demonstration of a biological role for D-DT, and its synergism with MIF suggests that the combined therapeutic targeting of both family members may enhance current anti-MIF-based therapies.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell LineCell Line, TumorHumansInterleukin-8Intramolecular OxidoreductasesLung NeoplasmsMacrophage Migration-Inhibitory FactorsMiceNeovascularization, PathologicVascular Endothelial Growth Factor ACXCL8 protein, humandopachrome isomeraseInterleukin-8Intramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMIF protein, humanVascular Endothelial Growth Factor A

Identifiers

PMID18684922
PMCPMC2709419
OpenAlexW2102590613

What OpenQuestion holds

Textmetadata
LicenceTDM
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.