Evidence map›Paper›PMID 21163944›Full record

ArticleThe Journal of biological chemistry2011

Kallikrein-5 promotes cleavage of desmoglein-1 and loss of cell-cell cohesion in oral squamous cell carcinoma.

Rong Jiang, Zonggao Shi, Jeffrey J Johnson, Yueying Liu, M Sharon Stack

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

35 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Eosinophilic esophagitis: Immune mechanisms and therapeutic targets.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2022
    Review
  10. Review
  11. Desmosomal Cadherins in Health and Disease.Annual review of pathology · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

5 authors.

Rong JiangDepartment of Pathology and Anatomical Science, University of Missouri School of Medicine, Columbia, Missouri 65212, USA.
Zonggao Shi
Jeffrey J Johnson
Yueying Liu
M Sharon Stack

Funding

Interaction of uPAR & Integrins in Oral CancerR01CA085870 · NCI · UNIVERSITY OF NOTRE DAME · PI STACK, MARY SHARON · 2001 to 2010
$2.1M
NCI NIH HHS CA085870NCI NIH HHS R01 CA085870
6 · The paper itself

Abstract

Oral squamous cell carcinoma (OSCC) ranks among the top 8 causes of cancer death worldwide, with only a 60% 5-year survival rate, highlighting the need for discovery of novel biomarkers and therapeutic targets. We have previously reported that expression of a panel of serine proteinase kallikreins (KLK 5, 7, 8, and 10) is correlated with formation of more aggressive OSCC tumors in a murine orthotopic OSCC model and is elevated in human OSCC. Current studies focus on understanding the potential role of KLK5 in OSCC progression. In initial studies, KLK levels in malignant OSCC cells (SCC25) were compared with cells from normal oral mucosa (OKF/6) and pre-malignant oral keratinocytes (pp126) using qPCR. A marked elevation of all KLKs was observed in aggressive SCC25 cells relative to OKF/6 cells. In normal skin, KLKs are involved in desquamation during epidermal differentiation via proteolytic cleavage of the desmosomal cadherin component desmoglein 1 (Dsg1). As loss of cell-cell cohesion is prevalent in tumor metastasis, Dsg1 integrity was evaluated. Results show that SCC25 cells exhibit cleavage of Dsg1, which is blocked by proteinase inhibitor treatment as well as by siRNA silencing of KLK5 expression. Furthermore, cell-cell aggregation assays demonstrate that silencing of KLK5 enforces cell-cell adhesion; conversely, overexpression of KLK5 in normal oral mucosal cells (OKF/6) enhances cell dispersal. These data suggest that KLK5 may promote metastatic dissemination of OSCC by promoting loss of junctional integrity through cleavage of desmoglein 1.

Indexed as

AnimalsCarcinoma, Squamous CellCell AdhesionCell Line, TransformedCell Line, TumorDesmoglein 1Gene SilencingHumansKallikreinsMiceNeoplasm MetastasisNeoplasm ProteinsTongue NeoplasmsDesmoglein 1DSG1 protein, humanKallikreinsKLK5 protein, humanNeoplasm Proteins

Identifiers

PMID21163944
PMCPMC3059049

What OpenQuestion holds

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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.