Evidence map›Paper›PMID 26959880›Full record

ArticleOncotarget2016

Prp19 facilitates invasion of hepatocellular carcinoma via p38 mitogen-activated protein kinase/twist1 pathway.

Jie Yin, Lan Wang, Ji-Min Zhu, Qian Yu, Ru-Yi Xue, Ying Fang, Yi-An Zhang, Yan-Jie Chen, Tao-Tao Liu, Ling Dong and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
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  13. [Research advances in epithelial - mesenchymal transition in hepatocellular carcinoma].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017
    Review
  14. Prp19 Arrests Cell Cycle via Cdc5L in Hepatocellular Carcinoma Cells.International journal of molecular sciences · 2017
    Article
  15. Article
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 3 institutions in 1 country.

Jie YinDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Lan WangDepartment of Biochemistry and Molecular Biology, Shanghai Medical College of Fudan University, Shanghai, China.
Ji-Min ZhuDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Qian YuDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Ru-Yi XueDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Ying FangDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Yi-An ZhangDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Yan-Jie ChenDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Tao-Tao LiuDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Ling DongDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Xi-Zhong ShenDepartment of Gastroenterology, Zhongshan Hospital of Fudan University, Shanghai, China.
Zhongshan Hospital · CNFudan University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pre-mRNA processing factor 19 (Prp19) is involved in many cellular events including pre-mRNA processing and DNA damage response. However, the pathological role of Prp19 in hepatocellular carcinoma (HCC) is still elusive. Here, we reported that Prp19 was increased in most HCC tissues and HCC cell lines, and its overexpression in HCC tissues was positively correlated with vascular invasion, tumor capsule breakthrough and poor prognosis. Prp19 potentiated migratory and invasive abilities of HCC cells in vitro and in vivo. Furthermore Prp19 facilitated Twist1-induced epithelial-mesenchymal transition. Mechanistic insights revealed that Prp19 directly binded with TGF-β-activated kinase1 (TAK1) and promoted the activation of p38 mitogen-activated protein kinase (MAPK), preventing Twist1 from degradation. Finally Prp19/p38 MAPK/Twist1 axis was attested in nude mice xenografts and HCC patient specimens. This work implies that the gain of Prp19 is a critical event during the progression of HCC, making it a promising target for malignancies with aberrant Prp19 expression.

Indexed as

AnimalsCarcinoma, HepatocellularDisease ProgressionDNA Repair EnzymesEpithelial-Mesenchymal TransitionHeterograftsHumansKaplan-Meier EstimateLiver NeoplasmsMiceMice, NudeNeoplasm InvasivenessNuclear Proteinsp38 Mitogen-Activated Protein KinasesRNA Splicing FactorsTwist-Related Protein 1DNA Repair EnzymesNuclear Proteinsp38 Mitogen-Activated Protein KinasesPRPF19 protein, humanRNA Splicing FactorsTWIST1 protein, humanTwist-Related Protein 1liver cancersignaling pathwaytumor progressionubiquitination

Identifiers

PMID26959880
PMCPMC5008335
OpenAlexW2302060882

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.