Evidence map›Paper›PMID 21135113›Full record

ArticleCancer research2011

14-3-3sigma exerts tumor-suppressor activity mediated by regulation of COP1 stability.

Chun-Hui Su, Ruiying Zhao, Fanmao Zhang, Changju Qu, Bo Chen, Yin-Hsun Feng, Liem Phan, Jian Chen, Hua Wang, Huamin Wang and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

41 citing papers in PubMed, 57 citations in OpenAlex.

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  19. Essential Roles of E3 Ubiquitin Ligases in p53 Regulation.International journal of molecular sciences · 2017
    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

12 authors at 4 institutions in 3 countries.

Chun-Hui SuDepartment of Molecular and Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.
Ruiying Zhao
Fanmao Zhang
Changju Qu
Bo Chen
Yin-Hsun Feng
Liem Phan
Jian Chen
Hua Wang
Huamin Wang
Sai-Ching J Yeung
Mong-Hong Lee
China Medical University · TWChi Mei Medical Center · TWFirst Hospital of China Medical University · CNThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Regulation of cyclin-dependent kinase inhibitor p27 in cancerR01CA089266 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LEE, MONG-HONG · 2002 to 2013
$2.8M
Regulation of cyclin-dependent kinase inhibitor p27 in cancerR56CA089266 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LEE, MONG-HONG · 2008 to 2008
$276k
NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA089266NCI NIH HHS R01CA089266NCI NIH HHS R56 CA089266
6 · The paper itself

Abstract

Constitutive photomorphogenic 1 (COP1) is a p53-targeting E3 ubiquitin ligase that is downregulated by DNA damage through mechanisms that remain obscure. Here, we report that COP1 is not downregulated following DNA damage in 14-3-3σ null cells, implicating 14-3-3σ as a critical regulator in the response of COP1 to DNA damage. We also identified that 14-3-3σ, a p53 target gene product, interacted with COP1 and controlled COP1 protein stability after DNA damage. Mechanistic studies revealed that 14-3-3σ enhanced COP1 self-ubiquitination, thereby preventing COP1-mediated p53 ubiquitination, degradation, and transcriptional repression. In addition, we found that COP1 expression promoted cell proliferation, cell transformation, and tumor progression, manifesting its role in cancer promotion, whereas 14-3-3σ negatively regulated COP1 function and prevented tumor growth in a mouse xenograft model of human cancer. Immunohistochemical analysis of clinical breast and pancreatic cancer specimens demonstrated that COP1 protein levels were inversely correlated with 14-3-3σ protein levels. Together, our findings define a mechanism for posttranslational regulation of COP1 after DNA damage that can explain the correlation between COP1 overexpression and 14-3-3σ downregulation during tumorigenesis.

Indexed as

14-3-3 ProteinsAnimalsBiomarkers, TumorBreast NeoplasmsCell AdhesionCell Growth ProcessesCell Line, TumorColonic NeoplasmsDNA DamageDown-RegulationExonucleasesExoribonucleasesHCT116 CellsHumansMiceMice, Nude14-3-3 ProteinsBiomarkers, TumorCOP1 protein, humanExonucleasesExoribonucleasesSFN protein, humanTP53 protein, humanTumor Suppressor Protein p53Ubiquitin-Protein Ligases

Identifiers

PMID21135113
PMCPMC3358120
OpenAlexW1967703311

What OpenQuestion holds

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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.