Evidence map›Paper›PMID 25220593›Full record

ArticleNeoplasia (New York, N.Y.)2014

Late Cornified Envelope Group I, a novel target of p53, regulates PRMT5 activity.

Zhenzhong Deng, Koichi Matsuda, Chizu Tanikawa, Jiaying Lin, Yoichi Furukawa, Ryuji Hamamoto, Yusuke Nakamura

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 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

7 authors at 2 institutions in 2 countries.

Zhenzhong DengSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL 60637 USA; Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Koichi MatsudaLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Chizu TanikawaLaboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Jiaying LinSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL 60637 USA; Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yoichi FurukawaDivision of Clinical Genome Research, Advanced Clinical Research Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Ryuji HamamotoSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL 60637 USA.
Yusuke NakamuraSection of Hematology/Oncology, Department of Medicine, The University of Chicago, Chicago, IL 60637 USA. Electronic address: ynakamura@bsd.uchicago.edu.
The University of Tokyo · JPUniversity of Chicago · US

Funding

Re-Engineering Translational Research at the University of ChicagoUL1TR000430 · NCATS · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2012 to 2016
$20.2M
NCATS NIH HHS UL1 TR000430
6 · The paper itself

Abstract

p53 is one of the most important tumor suppressor genes involved in human carcinogenesis. Although downstream targets of p53 and their biologic functions in cancer cells have been extensively investigated, it is still far from the full understanding. Here, we demonstrate that Late Cornified Envelope Group I (LCE1) genes, which are located in the LCE gene clusters encoding multiple well-conserved stratum-corneum proteins, are novel downstream targets of p53. Exogenous p53 overexpression using an adenoviral vector system significantly enhanced the expression of LCE1 cluster genes. We also observed induction of LCE1 expressions by DNA damage, which was caused by treatment with adriamycin or UV irradiation in a wild-type p53-dependent manner. Concordantly, the induction of LCE1 by DNA damage was significantly attenuated by the knockdown of p53. Among predicted p53-binding sites within the LCE1 gene cluster, we confirmed one site to be a p53-enhancer sequence by reporter assays. Furthermore, we identified LCE1 to interact with protein arginine methyltransferase 5 (PRMT5). Knockdown of LCE1 by specific small interfering RNAs significantly increased the symmetric dimethylation of histone H3 arginine 8, a substrate of PRMT5, and overexpression of LCE1F remarkably decreased its methylation level. Our data suggest that LCE1 is a novel p53 downstream target that can be directly transactivated by p53 and is likely to have tumor suppressor functions through modulation of the PRMT5 activity.

Indexed as

Cell Line, TumorCornified Envelope Proline-Rich ProteinsGene ExpressionGene Expression Regulation, NeoplasticGenes, ReporterHumansModels, BiologicalMultigene FamilyProtein-Arginine N-MethyltransferasesProtein BindingProtein TransportTumor Suppressor Protein p53Cornified Envelope Proline-Rich ProteinsPRMT5 protein, humanProtein-Arginine N-MethyltransferasesTumor Suppressor Protein p53

Identifiers

PMID25220593
PMCPMC4234875
OpenAlexW2163345112

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.