Evidence map›Paper›PMID 28856538›Full record

ArticleDigestive diseases and sciences2017

UBR5 Contributes to Colorectal Cancer Progression by Destabilizing the Tumor Suppressor ECRG4.

Jin Wang, Xiaomu Zhao, Lan Jin, Guocong Wu, Yingchi Yang

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 48 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

5 authors at 2 institutions in 1 country.

Jin WangDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing, 100050, China. wangjin4632@163.com.
Xiaomu ZhaoDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
Lan JinDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
Guocong WuDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
Yingchi YangDepartment of General Surgery, Beijing Friendship Hospital, Capital Medical University, 95 Yongan Road, Xicheng District, Beijing, 100050, China.
Beijing Friendship Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe E3 ligase UBR5 is aberrantly expressed in diverse types of cancer. However, its expression pattern and biological function in colorectal cancer (CRC) remain unclear.

methodsWe used RT-PCR, Western blot, and immunohistochemistry to measure UBR5 expression in CRC tissues and corresponding non-tumor tissues. The expression pattern of UBR5 in CRC tissues was determined by scoring system of immunohistochemical analysis and mRNA level by RT-PCR. The statistical analyses were applied to evaluate the associations of UBR5 expression with survival rate of patients. The UBR5 gene was overexpressed or silenced with lentiviral vectors in CRC cells. And, cell proliferation and apoptosis were measured using CCK8 assay and flow cytometry.

resultsWe found that UBR5 is abundantly overexpressed in CRC tissues than adjacent non-cancerous tissues. We also found that high UBR5 level is positively correlated with progression and poor survival in CRC patients. In addition, further multivariate analysis indicated that UBR5 and TNM stage were independent prognostic factors for overall survival in patients with CRC. Furthermore, we demonstrated that the expression of UBR5 was significantly elevated in CRC cell lines. Overexpression of UBR5 enhanced in vitro cell proliferation and promoted in vivo tumor growth, whereas silencing UBR5 suppressed growth of CRC cells. Moreover, our findings show that UBR5 promotes CRC cell proliferation by inducing cell cycle progression and suppressing cell apoptosis. Finally, we found that UBR5 directly binds to the tumor suppressor esophageal cancer-related gene 4 (ECRG4) and increased its ubiquitination to reduce the protein stability of ECRG4.

conclusionsWe identified a tumorigenic role of UBR5 in CRC and provided a novel therapeutic target for CRC patients.

Indexed as

AnimalsApoptosisCell CycleCell ProliferationColorectal NeoplasmsFemaleGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansLogistic ModelsMaleMice, Inbred BALB CMice, NudeMiddle AgedECRG4 protein, humanNeoplasm ProteinsRNA, MessengerTumor Suppressor ProteinsUbiquitin-Protein LigasesUBR5 protein, humanApoptosisColorectal cancerECRG4ProliferationUBR5

Identifiers

PMID28856538
OpenAlexW2751161631

What OpenQuestion holds

Textmetadata
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.