Evidence map›Paper›PMID 26759305›Full record

ArticleJournal of experimental & clinical cancer research : CR2016

The human RNA surveillance factor UPF1 regulates tumorigenesis by targeting Smad7 in hepatocellular carcinoma.

Lei Chang, Cuicui Li, Tao Guo, Haitao Wang, Weijie Ma, Yufeng Yuan, Quanyan Liu, Qifa Ye, Zhisu Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

53 citing papers in PubMed, 78 citations in OpenAlex.

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  16. Inhibition of Nonsense-Mediated Decay Induces Nociceptive Sensitization through Activation of the Integrated Stress Response.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
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  17. 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

9 authors at 2 institutions in 1 country.

Lei ChangDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China. reniorchang@163.com.
Cuicui LiZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation Donghu Road 169, Wuhan, 430071, China. 1006672622@qq.com.
Tao GuoDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China. 345259934@qq.com.
Haitao WangDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China. wdevali@whu.edu.cn.
Weijie MaDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China. 469386903@qq.com.
Yufeng YuanDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China. yuanyf1971@163.com.
Quanyan LiuDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China. 407019815@qq.com.
Qifa YeZhongnan Hospital of Wuhan University, Institute of Hepatobiliary Diseases of Wuhan University, Transplant Center of Wuhan University, Hubei Key Laboratory of Medical Technology on Transplantation Donghu Road 169, Wuhan, 430071, China. whuyeqifa@163.com.
Zhisu LiuDepartment of General Surgery, Research Center of Digestive Diseases, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, China. liuzs53@163.com.
Wuhan University · CNZhongnan Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn spite of progress in diagnostics and treatment of Hepatocellular Carcinoma (HCC), its prognosis remains poor, and improved treatment strategies for HCC require detailed understanding of the underlying mechanism. In this investigation we studied the role of Up-frameshift 1 (UPF1) in the tumorigenesis of HCC.

methodsWe determined the expression level of UPF1 in HCC tissues with quantitative real-time PCR and western blotting and then studied its clinical significance. Sodium bisulfite sequencing was used to investigate the regulation of UPF1. We explored the biological significance of UPF1 with gain-and-loss-of-function analyses both in vitro and in vivo. The relationship between UPF1 and SMAD7 was also investigated by western blotting and immunofluorescence.

resultsA great downregulation of UPF1 due to promoter hypermethylation was observed in tumor tissues compared to their adjacent normal tissues. Meanwhile, patients with low UPF1 expression have significantly poorer prognosis than those with high expression. Functionally, UPF1 regulated HCC tumorigenesis both in vitro and in vivo. Moreover, the decreased UPF1 level in HCC reduces NMD efficiency and leads to up-regulation of Smad7, then affects the TGF-β pathway.

conclusionOur findings revealed that UPF1 is a potential tumor suppressive gene and may be a potential therapeutic target for HCC.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorDNA MethylationFemaleGene Expression Regulation, NeoplasticHep G2 CellsHumansLiver NeoplasmsMaleMicePrognosisPromoter Regions, GeneticRNA HelicasesSmad7 ProteinTrans-ActivatorsRNA HelicasesSmad7 ProteinSMAD7 protein, humanTrans-ActivatorsUPF1 protein, human

Identifiers

PMID26759305
PMCPMC4711019
OpenAlexW2236660254

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.