Evidence map›Paper›PMID 24457968›Full record

ArticleCell death & disease2014

OCT4 as a target of miR-34a stimulates p63 but inhibits p53 to promote human cell transformation.

W L Ng, G Chen, M Wang, H Wang, M Story, J W Shay, X Zhang, J Wang, A R M R Amin, B Hu and 2 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 6 institutions in 1 country.

W L NgDepartment of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, USA.
G ChenDepartment of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, USA.
M WangDivision of Space Life Sciences, Universities Space Research Association, Houston, TX, USA.
H WangDepartment of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, USA.
M StoryDepartment of Radiation Oncology, UT Southwestern Medical Center, Dallas, TX, USA.
J W ShayDepartment of Cell Biology, UT Southwestern Medical Center, Dallas, TX, USA.
X ZhangDepartment of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, USA.
J WangDepartment of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, USA.
A R M R AminDepartment of Hematology and Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, USA.
B Hu1] Department of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, USA [2] Department of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing, China.
F A CucinottaDepartment of Health Physics and Diagnostic Sciences, University of Nevada, Las Vegas, NV, USA.
Y WangDepartment of Radiation Oncology, Emory University School of Medicine, Winship Cancer Institute of Emory University, Atlanta, GA, USA.
Winship Cancer InstituteEmory University · USSouthwestern Medical CenterSouthwestern Medical Center · USUniversities Space Research Association · USUniversity of Nevada, Las Vegas · US

Funding

A new role of MEPE/OF45 as a co-factor of CHK1 for DNA damage responseR01GM080771 · NIGMS · THOMAS JEFFERSON UNIVERSITY · PI WANG, YA · 2007 to 2010
$1.4M
NIGMS NIH HHS GM080771NIGMS NIH HHS R01 GM080771
6 · The paper itself

Abstract

Human cell transformation is a key step for oncogenic development, which involves multiple pathways; however, the mechanism remains unclear. To test our hypothesis whether cell oncogenic transformation shares some mechanisms with the process of reprogramming non-stem cells to induced pluripotent stem cells (iPSC), we studied the relationship among the key factors for promoting or inhibiting iPSC in radiation-transformed human epithelial cell lines derived from different tissues (lung, breast and colon). We unexpectedly found that p63 and OCT4 were highly expressed (accompanied by low expressed p53 and miR-34a) in all transformed cell lines examined when compared with their non-transformed counterparts. We further elucidated the relationship of these factors: the 3p strand of miR-34a directly targeted OCT4 by binding to the 3' untranslated region (3'-UTR) of OCT4 and, OCT4, in turn, stimulated p63 but inhibited p53 expression by binding to a specific region of the p63 or p53 promoter. Moreover, we revealed that the effects of OCT4 on promoting cell oncogenic transformation were by affecting p63 and p53. These results support that a positive loop exists in human cells: OCT4 upregulation as a consequence of inhibition of miR-34a, promotes p63 but suppresses p53 expression, which further stimulates OCT4 upregulation by downregulating miR-34a. This functional loop contributes significantly to cell transformation and, most likely, also to the iPSC process.

Indexed as

Cell Transformation, NeoplasticGene Expression RegulationCell DifferentiationHumansInduced Pluripotent Stem CellsMicroRNAsOctamer Transcription Factor-3Promoter Regions, GeneticProtein BindingTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor ProteinsMicroRNAsMIRN34 microRNA, humanOctamer Transcription Factor-3POU5F1 protein, humanTP63 protein, humanTranscription FactorsTumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID24457968
PMCPMC4040665
OpenAlexW1993475172

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.