Evidence map›Paper›PMID 26190376›Full record

ArticleScientific reports2015

TMPRSS4 facilitates epithelial-mesenchymal transition of hepatocellular carcinoma and is a predictive marker for poor prognosis of patients after curative resection.

Cheng-Hao Wang, Zhong-Yi Guo, Ze-Ting Chen, Xu-Ting Zhi, Deng-Ke Li, Zhao-Ru Dong, Zhi-Qiang Chen, San-Yuan Hu, Tao Li

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

9 authors at 2 institutions in 1 country.

Cheng-Hao Wang1] Department of general surgery, Qilu Hospital, Shandong University, Jinan 250012, P.R.China [2] Liver Cancer Institute and Zhongshan Hospital, Fudan University, Key Laboratory for Carcinogenesis &Cancer Invasion, the Chinese Ministry of Education, Shanghai 200032, P.R.China.
Zhong-Yi GuoDepartment of general surgery, Qilu Hospital, Shandong University, Jinan 250012, P.R.China.
Ze-Ting ChenDepartment of general surgery, Qilu Hospital, Shandong University, Jinan 250012, P.R.China.
Xu-Ting ZhiDepartment of general surgery, Qilu Hospital, Shandong University, Jinan 250012, P.R.China.
Deng-Ke LiDepartment of general surgery, Qilu Hospital, Shandong University, Jinan 250012, P.R.China.
Zhao-Ru DongLiver Cancer Institute and Zhongshan Hospital, Fudan University, Key Laboratory for Carcinogenesis &Cancer Invasion, the Chinese Ministry of Education, Shanghai 200032, P.R.China.
Zhi-Qiang ChenDepartment of general surgery, Qilu Hospital, Shandong University, Jinan 250012, P.R.China.
San-Yuan HuDepartment of general surgery, Qilu Hospital, Shandong University, Jinan 250012, P.R.China.
Tao LiDepartment of general surgery, Qilu Hospital, Shandong University, Jinan 250012, P.R.China.
Qilu Hospital of Shandong University · CNZhongshan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TMPRSS4 (Transmembrane protease serine 4) is up-regulated in a broad spectrum of cancers. However, little is known about the biological effects of TMPRSS4 on hepatocellular carcinoma (HCC) and the related mechanisms. In the present study, we found that overexpression of TMPRSS4 significantly promoted the invasion, migration, adhesion and metastasis of HCC. Further more, TMPRSS4 induced EMT of HCC, which was mediated via snail and slug as a result of Raf/MEK/ERK1/2 activation, and inhibition of ERK1/2 activation by its inhibitor was associated with reduced cell invasion and reversion of EMT. In addition, we demonstrated that TMPRSS4 remarkably suppressed the expression of RECK, an inhibitor of angiogenesis, and drastically induced tumor angiogenesis and growth. More important, in clinical HCC specimens, TMPRSS4 expression was significantly correlated with tumor staging and was inversely correlated with E-cadherin and RECKS expression. Expression of TMPRSS4 is significantly associated with HCC progression and is an independent prognostic factor for postoperative worse survival and recurrence. In conclusion, TMPRSS4 functions as a positive regulator of Raf/MEK/ERK1/2 pathway and promotes HCC progression by inducing EMT and angiogenesis. The increase of TMPRSS4 expression may be a key event for HCC progression and may be regarded as a potential prognostic marker for HCC.

Indexed as

AdultAgedAnimalsCadherinsCarcinoma, HepatocellularCell AdhesionCell Line, TumorCell MovementDisease Models, AnimalEpithelial-Mesenchymal TransitionFemaleGene ExpressionGene Expression Regulation, NeoplasticGPI-Linked ProteinsHeterograftsHumansCadherinsGPI-Linked ProteinsMembrane ProteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3raf KinasesRECK protein, humanSerine EndopeptidasesTMPRSS4 protein, human

Identifiers

PMID26190376
PMCPMC4507176
OpenAlexW959537295

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.