Evidence map›Paper›PMID 37596305›Full record

ArticleScientific reports2023

Dynamic interplay between sortilin and syndecan-1 contributes to prostate cancer progression.

Joanna Lazniewska, Ka Lok Li, Ian R D Johnson, Alexandra Sorvina, Jessica M Logan, Carmela Martini, Courtney Moore, Ben S-Y Ung, Litsa Karageorgos, Shane M Hickey and 18 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

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  4. Deletions ofBiomolecules · 2025
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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

28 authors at 6 institutions in 2 countries.

Joanna LazniewskaClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia. joanna.lazniewska@unisa.edu.au.
Ka Lok LiClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Ian R D JohnsonClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Alexandra SorvinaClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Jessica M LoganClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Carmela MartiniClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Courtney MooreClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Ben S-Y UngClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Litsa KarageorgosClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Shane M HickeyClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Sarita PrabhakaranClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Jessica K HeatlieClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Robert D BrooksClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Chelsea HuzzellClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia.
Nicholas I WarnockCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, 5000, Australia.
Mark P WardDepartment of Histopathology, Trinity College Dublin, Dublin 8, Ireland.
Bashir MohammedDepartment of Histopathology, Trinity College Dublin, Dublin 8, Ireland.
Prerna TewariDepartment of Histopathology, Trinity College Dublin, Dublin 8, Ireland.
Cara MartinDepartment of Histopathology, Trinity College Dublin, Dublin 8, Ireland.
Sharon O'TooleDepartment of Histopathology, Trinity College Dublin, Dublin 8, Ireland.
Laura Bogue EdgertonDepartment of Histopathology, Trinity College Dublin, Dublin 8, Ireland.
Mark BatesDepartment of Histopathology, Trinity College Dublin, Dublin 8, Ireland.
Paul MorettiCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, 5000, Australia.
Stuart M PitsonCentre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, SA, 5000, Australia.
Stavros SelemidisSchool of Health and Biomedical Sciences, STEM College, RMIT University, Bundoora, VIC, 3083, Australia.
Lisa M ButlerSouth Australian ImmunoGENomics Cancer Institute and Freemasons Centre for Male Health and Wellbeing, University of Adelaide, Adelaide, SA, 5000, Australia.
John J O'LearyDepartment of Histopathology, Trinity College Dublin, Dublin 8, Ireland.
Douglas A BrooksClinical and Health Sciences, University of South Australia, Adelaide, SA, 5000, Australia. doug.brooks@unisa.edu.au.
University of South Australia · AUTrinity College Dublin · IEFlinders University · AURMIT University · AUSouth Australian Health and Medical Research Institute · AUSouth Australia Pathology · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) development and progression relies on the programming of glucose and lipid metabolism, and this involves alterations in androgen receptor expression and signalling. Defining the molecular mechanism that underpins this metabolic programming will have direct significance for patients with PCa who have a poor prognosis. Here we show that there is a dynamic balance between sortilin and syndecan-1, that reports on different metabolic phenotypes. Using tissue microarrays, we demonstrated by immunohistochemistry that sortilin was highly expressed in low-grade cancer, while syndecan-1 was upregulated in high-grade disease. Mechanistic studies in prostate cell lines revealed that in androgen-sensitive LNCaP cells, sortilin enhanced glucose metabolism by regulating GLUT1 and GLUT4, while binding progranulin and lipoprotein lipase (LPL) to limit lipid metabolism. In contrast, in androgen-insensitive PC3 cells, syndecan-1 was upregulated, interacted with LPL and colocalised with β

Indexed as

Prostatic NeoplasmsAndrogen AntagonistsAndrogensHumansIntegrin beta3MaleNeoplastic ProcessesProstateSortilinSyndecan-1Androgen AntagonistsAndrogensIntegrin beta3SortilinSyndecan-1

Identifiers

PMID37596305
PMCPMC10439187
OpenAlexW4385987731

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.