Evidence map›Paper›PMID 27886258›Full record

ArticleScientific reports2016

A holistic approach to dissecting SPARC family protein complexity reveals FSTL-1 as an inhibitor of pancreatic cancer cell growth.

Katrina Viloria, Amanda Munasinghe, Sharan Asher, Roberto Bogyere, Lucy Jones, Natasha J Hill

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
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  9. Article
  10. Emerging Roles of Matricellular Proteins in Systemic Sclerosis.International journal of molecular sciences · 2020
    Review
  11. Article
  12. Article
  13. Epigenetic silencing ofOncotarget · 2018
    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

6 authors at 1 institution in 1 country.

Katrina ViloriaDepartment of Biomolecular Sciences, Kingston University, Kingston-upon-Thames, UK.
Amanda MunasingheDepartment of Biomolecular Sciences, Kingston University, Kingston-upon-Thames, UK.
Sharan AsherDepartment of Biomolecular Sciences, Kingston University, Kingston-upon-Thames, UK.
Roberto BogyereDepartment of Biomolecular Sciences, Kingston University, Kingston-upon-Thames, UK.
Lucy JonesDepartment of Biomolecular Sciences, Kingston University, Kingston-upon-Thames, UK.
Natasha J HillDepartment of Biomolecular Sciences, Kingston University, Kingston-upon-Thames, UK.
Kingston University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SPARC is a matricellular protein that is involved in both pancreatic cancer and diabetes. It belongs to a wider family of proteins that share structural and functional similarities. Relatively little is known about this extended family, but evidence of regulatory interactions suggests the importance of a holistic approach to their study. We show that Hevin, SPOCKs, and SMOCs are strongly expressed within islets, ducts, and blood vessels, suggesting important roles for these proteins in the normal pancreas, while FSTL-1 expression is localised to the stromal compartment reminiscent of SPARC. In direct contrast to SPARC, however, FSTL-1 expression is reduced in pancreatic cancer. Consistent with this, FSTL-1 inhibited pancreatic cancer cell proliferation. The complexity of SPARC family proteins is further revealed by the detection of multiple cell-type specific isoforms that arise due to a combination of post-translational modification and alternative splicing. Identification of splice variants lacking a signal peptide suggests the existence of novel intracellular isoforms. This study underlines the importance of addressing the complexity of the SPARC family and provides a new framework to explain their controversial and contradictory effects. We also demonstrate for the first time that FSTL-1 suppresses pancreatic cancer cell growth.

Indexed as

Alternative SplicingAnimalsCalcium-Binding ProteinsCell Line, TumorCell ProliferationDown-RegulationExtracellular Matrix ProteinsFollistatin-Related ProteinsGene Expression Regulation, NeoplasticHumansIslets of LangerhansMiceNeoplasm TransplantationPancreatic NeoplasmsProtein Processing, Post-TranslationalProteoglycansCalcium-Binding ProteinsExtracellular Matrix ProteinsFollistatin-Related ProteinsFSTL1 protein, humanProteoglycansSPARCL1 protein, humanSPOCK1 protein, human

Identifiers

PMID27886258
PMCPMC5122892
OpenAlexW2555344458

What OpenQuestion holds

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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.