Evidence map›Paper›PMID 24192928›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2014

Oncogenic function of SCCRO5/DCUN1D5 requires its Neddylation E3 activity and nuclear localization.

Claire C Bommeljé, Víola B Weeda, Guochang Huang, Kushyup Shah, Sarina Bains, Elizabeth Buss, Manish Shaha, Mithat Gönen, Ronald Ghossein, Suresh Y Ramanathan and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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  18. Neddylation E2 UBE2F Promotes the Survival of Lung Cancer Cells by Activating CRL5 to Degrade NOXA via the K11 Linkage.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
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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

11 authors at 1 institution in 1 country.

Claire C BommeljéAuthors' Affiliations: Department of Surgery, Laboratory of Epithelial Cancer Biology and Departments of Epidemiology and Biostatistics and Pathology, Memorial Sloan-Kettering Cancer Center, New York, New York.
Víola B Weeda
Guochang Huang
Kushyup Shah
Sarina Bains
Elizabeth Buss
Manish Shaha
Mithat Gönen
Ronald Ghossein
Suresh Y Ramanathan
Bhuvanesh Singh
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

purposeTo determine mechanisms by which SCCRO5 (aka DCUN1D5) promotes oncogenesis. EXPERIMENTAL

designSCCRO5 mRNA and protein expression were assessed in 203 randomly selected primary cancer tissue samples, matched histologically normal tissues, and cell lines by use of real-time PCR and Western blot analysis. SCCRO5 overexpression was correlated with survival. The effect of SCCRO5 knockdown on viability was assessed in selected cancer cell lines. Structure-function studies were performed to determine the SCCRO5 residues required for binding to the neddylation components, for neddylation-promoting activity, and for transformation.

resultsIn oral and lung squamous cell carcinomas, SCCRO5 mRNA levels corresponded with protein levels and overexpression correlated with decreased disease-specific survival. Knockdown of SCCRO5 by RNAi resulted in a selective decrease in the viability of cancer cells with high endogenous levels, suggesting the presence of oncogene addiction. SCCRO5 promoted cullin neddylation while maintaining conserved reaction processivity paradigms involved in ubiquitin and ubiquitin-like protein conjugation, establishing it as a component of the neddylation E3. Neddylation activities in vitro required the potentiating of neddylation (PONY) domain but not the nuclear localization sequence (NLS) domain. In contrast, both the NLS domain and the PONY domain were required for transformation of NIH-3T3 cells.

conclusionsOur data suggest that SCCRO5 has oncogenic potential that requires its function as a component of the neddylation E3. Neddylation activity and nuclear localization of SCCRO5 are important for its in vivo function.

Indexed as

AnimalsCell LineCell NucleusCell ProliferationCell Transformation, NeoplasticCullin ProteinsDisease ProgressionGene ExpressionHumansMiceNeoplasmsOncogene ProteinsPeptide SynthasesPhenotypeProtein BindingProtein TransportCullin ProteinsDCUN1D5 protein, humanOncogene ProteinsPeptide SynthasesUbiquitin-Protein LigasesUbiquitins

Identifiers

PMID24192928
PMCPMC4191716
OpenAlexW2158480811

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.