Evidence map›Paper›PMID 19555470›Full record

ArticleBMC cancer2009

Expression of prostasin and its inhibitors during colorectal cancer carcinogenesis.

Joanna Selzer-Plon, Jette Bornholdt, Stine Friis, Hanne C Bisgaard, Inger Mb Lothe, Kjell M Tveit, Elin H Kure, Ulla Vogel, Lotte K Vogel

Abstract read
In one paragraph

Article in BMC cancer, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Expression pattern of humanOncology letters · 2018
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. DNA Methylation Profiles of Protease Nexin 1 (SERPINE2) Gene in Human Cell Lines.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2011
    Article
  18. Article
  19. Article
  20. Membrane-anchored serine proteases in health and disease.Progress in molecular biology and translational science · 2011
    Review
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.

Joanna Selzer-PlonDepartment of Cellular and Molecular Medicine, Faculty of Health Science, University of Copenhagen, Denmark. selzer@sund.ku.dk
Jette Bornholdt
Stine Friis
Hanne C Bisgaard
Inger Mb Lothe
Kjell M Tveit
Elin H Kure
Ulla Vogel
Lotte K Vogel

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClinical trials where cancer patients were treated with protease inhibitors have suggested that the serine protease, prostasin, may act as a tumour suppressor. Prostasin is proteolytically activated by the serine protease, matriptase, which has a very high oncogenic potential. Prostasin is inhibited by protease nexin-1 (PN-1) and the two isoforms encoded by the mRNA splice variants of hepatocyte growth factor activator inhibitor-1 (HAI-1), HAI-1A, and HAI-1B.

methodsUsing quantitative RT-PCR, we have determined the mRNA levels for prostasin and PN-1 in colorectal cancer tissue (n = 116), severe dysplasia (n = 13), mild/moderate dysplasia (n = 93), and in normal tissue from the same individuals. In addition, corresponding tissues were examined from healthy volunteers (n = 23). A part of the cohort was further analysed for the mRNA levels of the two variants of HAI-1, here denoted HAI-1A and HAI-1B. mRNA levels were normalised to beta-actin. Immunohistochemical analysis of prostasin and HAI-1 was performed on normal and cancer tissue.

resultsThe mRNA level of prostasin was slightly but significantly decreased in both mild/moderate dysplasia (p < 0.001) and severe dysplasia (p < 0.01) and in carcinomas (p < 0.05) compared to normal tissue from the same individual. The mRNA level of PN-1 was more that two-fold elevated in colorectal cancer tissue as compared to healthy individuals (p < 0.001) and elevated in both mild/moderate dysplasia (p < 0.01), severe dysplasia (p < 0.05) and in colorectal cancer tissue (p < 0.001) as compared to normal tissue from the same individual. The mRNA levels of HAI-1A and HAI-1B mRNAs showed the same patterns of expression. Immunohistochemistry showed that prostasin is located mainly on the apical plasma membrane in normal colorectal tissue. A large variation was found in the degree of polarization of prostasin in colorectal cancer tissue.

conclusionThese results show that the mRNA level of PN-1 is significantly elevated in colorectal cancer tissue. Future studies are required to clarify whether down-regulation of prostasin activity via up regulation of PN-1 is causing the malignant progression or if it is a consequence of it.

Indexed as

Gene Expression Regulation, NeoplasticAgedAlternative SplicingAmyloid beta-Protein PrecursorCarcinomaCohort StudiesColorectal NeoplasmsFemaleHumansMaleMiddle AgedProstasinProtease NexinsProteinase Inhibitory Proteins, SecretoryProtein IsoformsReceptors, Cell SurfaceAmyloid beta-Protein PrecursorProstasinProtease NexinsProteinase Inhibitory Proteins, SecretoryProtein IsoformsReceptors, Cell SurfaceRNA, MessengerSerine EndopeptidasesSerpin E2SERPINE2 protein, humanSPINT1 protein, human

Identifiers

PMID19555470
PMCPMC2717118

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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.