Evidence map›Paper›PMID 27452522›Full record

ArticleOncogene2017

FOXM1 allows human keratinocytes to bypass the oncogene-induced differentiation checkpoint in response to gain of MYC or loss of p53.

R Molinuevo, A Freije, I de Pedro, S W Stoll, J T Elder, A Gandarillas

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  14. The Dominant Role of Forkhead Box Proteins in Cancer.International journal of molecular sciences · 2018
    Review
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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

6 authors at 4 institutions in 3 countries.

R MolinuevoCell Cycle, Stem Cell Fate and Cancer Laboratory, Institute of Research Marqués de Valdecilla (IDIVAL), Santander, Spain.
A FreijeCell Cycle, Stem Cell Fate and Cancer Laboratory, Institute of Research Marqués de Valdecilla (IDIVAL), Santander, Spain.
I de PedroCell Cycle, Stem Cell Fate and Cancer Laboratory, Institute of Research Marqués de Valdecilla (IDIVAL), Santander, Spain.
S W StollDepartment of Dermatology, University of Michigan, Ann Arbor, MI, USA.
J T ElderDepartment of Dermatology, University of Michigan, Ann Arbor, MI, USA.
A GandarillasCell Cycle, Stem Cell Fate and Cancer Laboratory, Institute of Research Marqués de Valdecilla (IDIVAL), Santander, Spain.
Instituto de Investigación Marqués de Valdecilla · ESInserm · FRUniversity of Michigan–Ann Arbor · USVA Ann Arbor Healthcare System · US

Funding

Amphiregulin in Psoriatic Epidermal HyperplasiaR01AR052889 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELDER, JAMES TILFORD · 2006 to 2010
$1.4M
Metalloproteinase regulation of ErbB signaling in skinR03AR049420 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STOLL, STEFAN W · 2004 to 2006
$227k
NIAMS NIH HHS R01 AR052889NIAMS NIH HHS R03 AR049420
6 · The paper itself

Abstract

Tumour suppressor p53 or proto-oncogene MYC is frequently altered in squamous carcinomas, but this is insufficient to drive carcinogenesis. We have shown that overactivation of MYC or loss of p53 via DNA damage triggers an anti-oncogenic differentiation-mitosis checkpoint in human epidermal keratinocytes, resulting in impaired cell division and squamous differentiation. Forkhead box M1 (FOXM1) is a transcription factor recently proposed to govern the expression of a set of mitotic genes. Deregulation of FOXM1 occurs in a wide variety of epithelial malignancies. We have ectopically expressed FOXM1 in keratinocytes of the skin after overexpression of MYC or inactivation of endogenous p53. Ectopic FOXM1 rescues the proliferative capacity of MYC- or p53-mutant cells in spite of higher genetic damage and a larger cell size typical of differentiation. As a consequence, differentiation induced by loss of p53 or MYC is converted into increased proliferation and keratinocytes displaying genomic instability are maintained within the proliferative compartment. The results demonstrate that keratinocyte oncogene-induced differentiation is caused by mitosis control and provide new insight into the mechanisms driving malignant progression in squamous cancer.

Indexed as

Cell DifferentiationCell ProliferationApoptosisCell CycleCells, CulturedForkhead Box Protein M1Genomic InstabilityHumansKeratinocytesMitosisOncogenesProto-Oncogene MasProto-Oncogene Proteins c-mycTumor Suppressor Protein p53Forkhead Box Protein M1FOXM1 protein, humanMAS1 protein, humanMYC protein, humanProto-Oncogene MasProto-Oncogene Proteins c-mycTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID27452522
PMCPMC5318665
OpenAlexW2488519071

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.