Evidence map›Paper›PMID 28771228›Full record

ArticleCell death & disease2017

Uev1A facilitates osteosarcoma differentiation by promoting Smurf1-mediated Smad1 ubiquitination and degradation.

Weiwei Zhang, Yuan Zhuang, Yiran Zhang, Xiaoran Yang, Hong Zhang, Guifen Wang, Wanqi Yin, Ruifeng Wang, Zhiling Zhang, Wei Xiao

Abstract read
In one paragraph

Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

10 authors.

Weiwei ZhangCollege of Life Sciences, Capital Normal University, Beijing, China.
Yuan ZhuangCollege of Life Sciences, Capital Normal University, Beijing, China.
Yiran ZhangCollege of Life Sciences, Capital Normal University, Beijing, China.
Xiaoran YangCollege of Life Sciences, Capital Normal University, Beijing, China.
Hong ZhangCollege of Life Sciences, Capital Normal University, Beijing, China.
Guifen WangCollege of Life Sciences, Capital Normal University, Beijing, China.
Wanqi YinCollege of Life Sciences, Capital Normal University, Beijing, China.
Ruifeng WangCollege of Life Sciences, Capital Normal University, Beijing, China.
Zhiling ZhangCollege of Life Sciences, Capital Normal University, Beijing, China.
Wei XiaoCollege of Life Sciences, Capital Normal University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant bone tumor osteosarcoma (OS) displays high metastasis incidence and poor prognosis. Its stem cell properties could serve to explain tumor recurrence and resistance to conventional treatments. In this study, we identified UEV1A as a novel suppressor of OS. Elevated UEV1A diminishes stem cell properties of OS cells and drives them to terminal differentiation. Importantly, UEV1A-overexpressed OS cells delay proliferation and are more sensitive to chemotherapeutic agents than control cells. Uev1A appears to be involved in the BMP signaling pathway in which it collaborates with a ubiquitin E3 ligase Smurf1 to promote Smad1 degradation in a Ubc13-independent manner. Indeed, Smad1 is identified as a dominant downstream effector of Uev1A, which unravels the mechanism underlying Uev1A-orchestrated tumor suppression in OS. The above findings identify UEV1A as a potential OS tumor suppression gene, and shed lights to future OS diagnosis and treatment.

Indexed as

Cell DifferentiationProteolysisUbiquitinationBone NeoplasmsCell Line, TumorHumansOsteosarcomaReceptors, LDLTranscription FactorsTumor Suppressor ProteinsUbiquitin-Conjugating EnzymesUbiquitin-Protein LigasesReceptors, LDLSAMD1 protein, humanSMURF1 protein, humanTranscription FactorsTumor Suppressor ProteinsUBE2V1 protein, humanUbiquitin-Conjugating EnzymesUbiquitin-Protein Ligases

Identifiers

PMID28771228
PMCPMC5596555

What OpenQuestion holds

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LicenceCC BY
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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.