Evidence map›Paper›PMID 31911755›Full record

ArticleCancer cell international2020

UBQLN4 promotes progression of HCC via activating wnt-β-catenin pathway and is regulated by miR-370.

Yan Yu, Penglin Xu, Guangying Cui, Xiaodong Xu, Kongfei Li, Xiaolong Chen, Jie Bao

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-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

22 citing papers in PubMed, 26 citations in OpenAlex.

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  16. UpregulatingJournal of Cancer · 2021
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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 1 country.

Yan Yu *1Precision Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052 China.
Penglin Xu *2Key Laboratory of Clinical Medicine, Department of Digestive Diseases, The First Affiliated Hospital of Zhengzhou University, 1# Jianshe East Road, Zhengzhou, 450052 China.
Guangying Cui1Precision Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052 China.
Xiaodong Xu2Key Laboratory of Clinical Medicine, Department of Digestive Diseases, The First Affiliated Hospital of Zhengzhou University, 1# Jianshe East Road, Zhengzhou, 450052 China.
Kongfei Li3Department of Hematology, Yinzhou People's Hospital Affiliated to Medical College of Ningbo University, Ningbo, China.
Xiaolong Chen1Precision Medicine Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052 China.
Jie Bao2Key Laboratory of Clinical Medicine, Department of Digestive Diseases, The First Affiliated Hospital of Zhengzhou University, 1# Jianshe East Road, Zhengzhou, 450052 China.ORCID 0000-0002-9145-9911
First Affiliated Hospital of Zhengzhou University · CNNingbo University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUbiquilin-4 (UBQLN4) is a member of the ubiquitin-proteasome system that is usually upregulated in many tumor cells. Its overexpression has been associated with poor disease outcomes in various cancer diseases. However, the underlying mechanism of UBQLN4 in the development of hepatocellular carcinoma (HCC) has not been elucidated.

methodsImmunochemistry, real-time PCR, and western blotting were used to evaluate the expression levels of UBQLN4 in cancer tissues. Univariate, Cox-regression, and Kaplan-Meier analyses were performed to determine the association between UBQLN4 expression and HCC prognosis. Cell Counting Kit-8 (CCK-8), transwell, EDU and colony formation assays were conducted to evaluate the role of UBQLN4 in HCC cell progression. The gene set enrichment analysis and luciferase reporter experiments were conducted to find the mechanism of UBQLN4 in HCC.

resultsUbiquilin-4 (UBQLN4) was overexpressed in HCC tissues. Besides, overexpression of UBQLN4 was associated with poor overall survival and disease-free survival rate of HCC patients. The loss-of-function analysis revealed that suppression of UBQLN4 inhibited the proliferation and invasion of HCC cells in vivo and in vitro. The KEGG (Kyoto Encyclopedia of Genes and Genomes) analysis showed that UBQLN4 could regulate activation of the wnt-β-catenin pathway in HCC cells. Furthermore, our results showed that UBQLN4 was downregulated by miR-370, which acted as a tumor suppressor gene in HCC progression.

conclusionThe results of the present study suggest that the miR-370/UBQLN4 axis may play a critical role in the progression of HCC. These findings may inform future strategies for the development of therapeutic agents against HCC.

Indexed as

Hepatocellular carcinoma (HCC)MiR-370Ubiquilin-4 (UBQLN4)wnt-β-catenin pathway

Identifiers

PMID31911755
PMCPMC6942288
OpenAlexW3005388847

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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.