Evidence map›Paper›PMID 19597474›Full record

ArticleOncogene2009

The role of SPARC in the TRAMP model of prostate carcinogenesis and progression.

N Said, H F Frierson, D Chernauskas, M Conaway, K Motamed, D Theodorescu

Abstract read
PubMed Publisher
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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 62 citations in OpenAlex.

  1. Trial
  2. Review
  3. Mechanisms Underlying the Rarity of Skeletal Muscle Cancers.International journal of molecular sciences · 2024
    Review
  4. Skin Cancer Microenvironment: What We Can Learn from Skin Aging?International journal of molecular sciences · 2023
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. SPARC regulates ferroptosis induced by sorafenib in human hepatocellular carcinoma.Cancer biomarkers : section A of Disease markers · 2021
    Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Re-sensitization of 5-FU resistance by SPARC through negative regulation of glucose metabolism in hepatocellular carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    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

6 authors at 1 institution in 1 country.

N SaidDepartment of Urology, University of Virginia, Charlottesville, VA 22908, USA.
H F Frierson
D Chernauskas
M Conaway
K Motamed
D Theodorescu
University of Virginia · US

Funding

VEGF, FAK and RAPP01CA104106 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI PASCHAL, BRYCE, THEODORESCU, DAN · 2005 to 2015
$17.9M
Understanding the RhoGDI2 metastasis suppressor geneR01CA143971 · NCI · UNIVERSITY OF COLORADO DENVER · PI THEODORESCU, DAN · 2010 to 2020
$4.4M
REGULATION OF FGF 2 MEDIATED ANGIOGENESIS BY SPARCK01CA089689 · NCI · THE HOPE HEART INSTITUTE · PI MOTAMED, KOUROS · 2001 to 2004
$561k
NCI NIH HHS CA104106NCI NIH HHS K01-CA089689NCI NIH HHS P01 CA104106NCI NIH HHS R01 CA143971
6 · The paper itself

Abstract

SPARC (Secreted Protein Acidic and Rich in Cysteine), is a matricellular glycoprotein that is produced by tumor and/or neighboring stroma. In human prostate cancer, SPARC immunoreactivity is highest in metastatic lesions but distinct contributions of tumoral and stromal SPARC to tumorigenesis and progression are unclear. To determine the role of SPARC in primary prostate tumorigenesis, we crossed SPARC-null (SP(-/-)) with TRAMP (Transgenic Adenocarcinoma of Mouse Prostate) mice. TRAMP(+)/SP(-/-) mice exhibited accelerated cancer development and progression. Compared to their TRAMP(+)/SP(-/-) counterparts, TRAMP(+)/SP(+/+) tumors had fewer proliferating cells, and decreased cyclins A and D1 with increased p21(Cip) and p27(Kip). Similar effects on proliferation and cell-cycle regulators were observed in human prostate cancer cell lines, transiently transfected with pSPARC. TRAMP(+)/SP(-/-) tumors exhibited decreased stromal collagen, enhanced matrix metalloproteinase activity and increased vascular endothelial growth factor, proinflammatory cytokines. To determine the contribution of stromal SPARC, we evaluated subcutaneous tumor growth of TRAMP cell lines in syngeneic SP(+/+) and SP(-/-) mice. Enhanced growth, decreased stromal collagen and increased proteolysis were noted in SP(-/-) mice. Our findings demonstrate that both tumor and stromal SPARC are limiting for primary prostate tumorigenesis and progression, through effects on the cell cycle and the creation of a less favorable tumor microenvironment.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCell Cycle ProteinsCollagenHumansMaleMiceMice, Inbred C57BLMice, TransgenicNeoplasm MetastasisOsteonectinProstatic NeoplasmsCell Cycle ProteinsCollagenOsteonectin

Identifiers

PMID19597474
OpenAlexW2018301474

What OpenQuestion holds

Textmetadata
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.