Evidence map›Paper›PMID 30755669›Full record

ArticleScientific reports2019

PRSS3/Mesotrypsin and kallikrein-related peptidase 5 are associated with poor prognosis and contribute to tumor cell invasion and growth in lung adenocarcinoma.

Honghai Ma, Alexandra Hockla, Christine Mehner, Matt Coban, Niv Papo, Derek C Radisky, Evette S Radisky

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Mouse model suggests limited role for human mesotrypsin in pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2021
    Article
  18. Article
  19. 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 2 institutions in 3 countries.

Honghai MaDepartment of Cancer Biology, Mayo Clinic, Jacksonville, FL, 32224, USA.
Alexandra HocklaDepartment of Cancer Biology, Mayo Clinic, Jacksonville, FL, 32224, USA.
Christine MehnerDepartment of Cancer Biology, Mayo Clinic, Jacksonville, FL, 32224, USA.
Matt CobanDepartment of Cancer Biology, Mayo Clinic, Jacksonville, FL, 32224, USA.
Niv PapoDepartment of Biotechnology Engineering and the National Institute of Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Derek C RadiskyDepartment of Cancer Biology, Mayo Clinic, Jacksonville, FL, 32224, USA. radisky.derek@mayo.edu.
Evette S RadiskyDepartment of Cancer Biology, Mayo Clinic, Jacksonville, FL, 32224, USA. radisky.evette@mayo.edu.
Mayo Clinic in Florida · USBen-Gurion University of the Negev · IL

Funding

Inhibiting serine protease-induced prostate cancer progressionR01CA154387 · NCI · MAYO CLINIC JACKSONVILLE · PI RADISKY, EVETTE S · 2013 to 2017
$1.6M
NCI NIH HHS R01 CA154387
6 · The paper itself

Abstract

Serine proteases have been implicated as key drivers and facilitators of lung cancer malignancy, and while these proteins represent straightforward targets for therapeutic inhibitors, identification of optimal points for intervention has been complicated by the complex networks in which these enzymes function. Here we implicate a signaling pathway consisting of PRSS3/mesotrypsin and kallikrein-related peptidase 5 (KLK5) in lung adenocarcinoma malignancy. We show that elevated PRSS3/mesotrypsin expression is prognostic for poor outcome for patients with lung adenocarcinoma, and that genetic or pharmacologic targeting of PRSS3/mesotrypsin reduces lung adenocarcinoma cell invasiveness and proliferation. We further show that genetic targeting of KLK5, a known target of PRSS3/mesotrypsin, phenocopies the effect of PRSS3/mesotrypsin knockdown, and also that elevated expression of KLK5 is similarly prognostic for outcome in lung adenocarcinoma. Finally, we use transcriptional profiling experiments to show that PRSS3/mesotrypsin and KLK5 control a common malignancy-promoting pathway. These experiments implicate a potential PRSS3/mesotrypsin-KLK5 signaling module in lung adenocarcinoma and reveal the potential therapeutic benefit of selectively targeting these pathways.

Indexed as

Adenocarcinoma of LungCarcinogenesisCell Growth ProcessesCell Line, TumorCell MovementGene Expression Regulation, NeoplasticHumansKallikreinsLung NeoplasmsMicroarray AnalysisNeoplasm InvasivenessPrognosisRNA, Small InterferingTrypsinKallikreinsKLK5 protein, humanPRSS3 protein, humanRNA, Small InterferingTrypsin

Identifiers

PMID30755669
PMCPMC6372636
OpenAlexW2914451427

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.