Evidence map›Paper›PMID 32290402›Full record

ReviewInternational journal of molecular sciences2020

Dysregulation of Type II Transmembrane Serine Proteases and Ligand-Dependent Activation of MET in Urological Cancers.

Shoichiro Mukai, Koji Yamasaki, Masato Fujii, Takahiro Nagai, Naoki Terada, Hiroaki Kataoka, Toshiyuki Kamoto

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Prognostic value of hepatocyte growth factor for muscle-invasive bladder cancer.Journal of cancer research and clinical oncology · 2022
    Article
  10. Review
  11. Review
  12. HGF/c-Met: A Key Promoter in Liver Regeneration.Frontiers in pharmacology · 2022
    Review
  13. Article
  14. 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

7 authors at 1 institution in 1 country.

Shoichiro MukaiDepartment of Urology, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, Japan.
Koji YamasakiDepartment of Urology, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, Japan.
Masato FujiiDepartment of Urology, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, Japan.
Takahiro NagaiDepartment of Urology, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, Japan.
Naoki TeradaDepartment of Urology, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, Japan.
Hiroaki KataokaOncopathology and Regenerative Biology Section, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, Japan.ORCID 0000-0001-9948-0451
Toshiyuki KamotoDepartment of Urology, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, Japan.
University of Miyazaki · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unlike in normal epithelium, dysregulated overactivation of various proteases have been reported in cancers. Degradation of pericancerous extracellular matrix leading to cancer cell invasion by matrix metalloproteases is well known evidence. On the other hand, several cell-surface proteases, including type II transmembrane serine proteases (TTSPs), also induce progression through activation of growth factors, protease activating receptors and other proteases. Hepatocyte growth factor (HGF) known as a multifunctional growth factor that upregulates cancer cell motility, invasiveness, proliferative, and anti-apoptotic activities through phosphorylation of MET (a specific receptor of HGF). HGF secreted as inactive zymogen (pro-HGF) from cancer associated stromal fibroblasts, and the proteolytic activation by several TTSPs including matriptase and hepsin is required. The activation is strictly regulated by HGF activator inhibitors (HAIs) in physiological condition. However, downregulation is frequently observed in cancers. Indeed, overactivation of MET by upregulation of matriptase and hepsin accompanied by the downregulation of HAIs in urological cancers (prostate cancer, renal cell carcinoma, and bladder cancer) are also reported, a phenomenon observed in cancer cells with malignant phenotype, and correlated with poor prognosis. In this review, we summarized current reports focusing on TTSPs, HAIs, and MET signaling axis in urological cancers.

Indexed as

AnimalsCell Line, TumorCell MembraneDisease SusceptibilityEnzyme ActivationHepatocyte Growth FactorHumansLigandsMembrane ProteinsProtein BindingProtein Interaction Domains and MotifsProto-Oncogene Proteins c-metSerine ProteasesSignal TransductionUrologic NeoplasmsHepatocyte Growth FactorLigandsMembrane ProteinsProto-Oncogene Proteins c-metSerine Proteasesbladder cancerhepatocyte growth factor (HGF)hepsinHGF activator inhibitor (HAI)matriptaseMETprostate cancerrenal cell carcinoma

Identifiers

PMID32290402
PMCPMC7215454
OpenAlexW3016143047

What OpenQuestion holds

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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.