Evidence map›Paper›PMID 19597471›Full record

ArticleOncogene2009

Lysyl oxidase propeptide inhibits prostate cancer cell growth by mechanisms that target FGF-2-cell binding and signaling.

A H Palamakumbura, S R Vora, M A Nugent, K H Kirsch, G E Sonenshein, P C Trackman

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Fibrosis and cancer: A strained relationship.Biochimica et biophysica acta. Reviews on cancer · 2020
    Review
  12. Article
  13. Article
  14. YAP/TAZ Related BioMechano Signal Transduction and Cancer Metastasis.Frontiers in cell and developmental biology · 2019
    Review
  15. Article
  16. Article
  17. Review
  18. Functional importance of lysyl oxidase family propeptide regions.Journal of cell communication and signaling · 2018
    Review
  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

6 authors at 1 institution in 1 country.

A H PalamakumburaDepartment of Periodontology and Oral Biology, Boston University Henry M Goldman School of Dental Medicine, MA 02118, USA.
S R Vora
M A Nugent
K H Kirsch
G E Sonenshein
P C Trackman
Boston University · US

Funding

GROWTH FACTORS AND GINGIVAL FIBROSISR01DE011004 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI TRACKMAN, PHILIP C · 2002 to 2011
$3.1M
Inhibited Intramembranous Bone Healing in DiabetesR01DE014066 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI TRACKMAN, PHILIP C · 2003 to 2013
$3.0M
NFKB/REL AND THE PATHOGENESIS OF BREAST CANCERR01CA082742 · NCI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SONENSHEIN, GAIL E. · 1999 to 2008
$2.2M
NCI NIH HHS CA082742NCI NIH HHS R01 CA082742NIDCR NIH HHS DE14066NIDCR NIH HHS R01 DE011004NIDCR NIH HHS R01 DE014066
6 · The paper itself

Abstract

Enhanced RAS signaling and decreased androgen dependence of prostate cancer cells accompany poor clinical outcomes. Elevated autocrine fibroblast growth factors 2 (FGF-2) signaling promotes prostate cancer cell growth and survival. Expression of lysyl oxidase (LOX) inhibits RAS transforming activity. LOX is secreted as 50 kDa pro-LOX protein and then undergoes extracellular proteolytic processing to form approximately 30 kDa LOX enzyme and approximately 18 kDa propeptide (LOX-PP). We have previously shown that LOX-PP inhibits breast cancer cell transformation and tumor formation, but mechanisms of action of LOX-PP have not been fully elucidated. Here we report that LOX expression is reduced in prostate cancer cell lines and that recombinant LOX-PP protein inhibits serum-stimulated DNA synthesis and MEK/ERK and PI3K/AKT pathways in DU 145 and PC-3 androgen-independent cell lines. In DU 145 cells, treatment with a pharmacologic FGF-receptor inhibitor or a neutralizing anti-FGFR1 antibody mimicked LOX-PP inhibition of serum-stimulated DNA synthesis. FGF-2-stimulated DNA synthesis, ERK1/2, AKT and FRS2alpha activation were found all to be inhibited by LOX-PP in DU 145 cells. LOX-PP reduced specific binding of FGF-2 to DU 145 cells, suggesting that LOX-PP targets FGF signaling at the receptor. Interestingly, PC-3 cells did not respond to FGF-2, consistent with previous reports. We conclude that LOX-PP inhibits proliferation of DU 145 cells by interfering with FGFR(s) binding and signaling, and that LOX-PP has other mechanisms of action in PC-3 cells.

Indexed as

Signal TransductionCell Line, TumorCell ProliferationDNAEnzyme PrecursorsFibroblast Growth Factor 2HumansMaleProstateProstatic NeoplasmsProtein-Lysine 6-OxidaseReceptors, Fibroblast Growth FactorRecombinant ProteinsDNAEnzyme PrecursorsFibroblast Growth Factor 2Protein-Lysine 6-OxidaseReceptors, Fibroblast Growth FactorRecombinant Proteins

Identifiers

PMID19597471
PMCPMC2753565
OpenAlexW1965148579

What OpenQuestion holds

Textmetadata
LicenceTDM
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.