Evidence map›Paper›PMID 24932684›Full record

ArticlePloS one2014

MIF family members cooperatively inhibit p53 expression and activity.

Stephanie E Brock, Beatriz E Rendon, Dan Xin, Kavitha Yaddanapudi, Robert A Mitchell

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Stephanie E BrockMolecular Targets Program, James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky, United States of America.
Beatriz E RendonMolecular Targets Program, James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky, United States of America.
Dan XinMolecular Targets Program, James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky, United States of America.
Kavitha YaddanapudiMolecular Targets Program, James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky, United States of America.
Robert A MitchellMolecular Targets Program, James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky, United States of America.
University of Louisville · US

Funding

Role of MIF in Rb inactivation and TumorigenesisR01CA102285 · NCI · UNIVERSITY OF LOUISVILLE · PI MITCHELL, ROBERT A · 2004 to 2009
$1.4M
NCI NIH HHS CA102285NCI NIH HHS R01 CA102285
6 · The paper itself

Abstract

The tumor suppressor p53 is induced by genotoxic stress in both normal and transformed cells and serves to transcriptionally coordinate cell cycle checkpoint control and programmed cell death responses. Macrophage migration inhibitory factor (MIF) is an autocrine and paracrine acting cytokine/growth factor that promotes lung adenocarcinoma cell motility, anchorage-independence and neo-angiogenic potential. Several recent studies indicate that the only known homolog of MIF, D-dopachrome tautomerase (D-DT - also referred to as MIF-2), has functionally redundant activities with MIF and cooperatively promotes MIF-dependent pro-tumorigenic phenotypes. We now report that MIF and D-DT synergistically inhibit steady state p53 phosphorylation, stabilization and transcriptional activity in human lung adenocarcinoma cell lines. The combined loss of MIF and D-DT by siRNA leads to dramatically reduced cell cycle progression, anchorage independence, focus formation and increased programmed cell death when compared to individual loss of MIF or D-DT. Importantly, p53 mutant and p53 null lung adenocarcinoma cell lines were only nominally rescued from the cell growth effects of MIF/D-DT combined deficiency suggesting only a minor role for p53 in these transformed cell growth phenotypes. Finally, increased p53 activation was found to be independent of aberrantly activated AMP-activated protein kinase (AMPK) that occurs in response to MIF/D-DT-deficiency but is dependent on reactive oxygen species (ROS) that mediate aberrant AMPK activation in these cells. Combined, these findings suggest that both p53 wildtype and mutant human lung adenocarcinoma tumors rely on MIF family members for maximal cell growth and survival.

Indexed as

AMP-Activated Protein KinasesCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell ProliferationCell SurvivalClone CellsHumansIntramolecular OxidoreductasesLung NeoplasmsMacrophage Migration-Inhibitory FactorsOxidation-ReductionOxidative StressPhenotypeTumor Suppressor Protein p53AMP-Activated Protein Kinasesdopachrome isomeraseIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsTumor Suppressor Protein p53

Identifiers

PMID24932684
PMCPMC4059697
OpenAlexW1972779738

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.