Evidence map›Paper›PMID 32896761›Full record

ArticleNeoplasia (New York, N.Y.)2020

Prostate cancer-derived MMP-3 controls intrinsic cell growth and extrinsic angiogenesis.

Jeremy S Frieling, Tao Li, Marilena Tauro, Conor C Lynch

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.6field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Hemorrhagic stroke-induced subtype of inflammatory reactive astrocytes disrupts blood-brain barrier.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  9. Article
  10. Article
  11. Liquid biopsy to personalize treatment for metastatic prostate cancer.American journal of translational research · 2024
    Review
  12. Article
  13. Review
  14. Review
  15. Wnt3a is a promising target in colorectal cancer.Medical oncology (Northwood, London, England) · 2023
    Review
  16. Review
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

Jeremy S FrielingDepartment of Tumor Biology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA.
Tao LiDepartment of Tumor Biology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA.
Marilena TauroDepartment of Tumor Biology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA.
Conor C LynchDepartment of Tumor Biology, H. Lee Moffitt Cancer Center & Research Institute, Tampa, FL 33612, USA. Electronic address: conor.lynch@moffitt.org.
Moffitt Cancer Center · US

Funding

Host MMP-mediated regulation of the vicious cycle of prostate to bone metastasesR01CA143094 · NCI · VANDERBILT UNIVERSITY · PI LYNCH, CONOR C · 2010 to 2014
$1.5M
NCI NIH HHS R01CA143094-CCL
6 · The paper itself

Abstract

Bone metastatic prostate cancer significantly impacts patient quality of life and overall survival, and despite available therapies, it is presently incurable with an unmet need for improved treatment options. As mediators of tumor progression, matrix metalloproteinases (MMPs) can degrade extracellular matrix components and regulate growth factor and cytokine bioactivity. Depending on tissue context, MMPs can either promote or inhibit tumorigenesis. Therefore, it is essential to study individual MMPs in specific cancer contexts and microenvironments to support the design and application of selective MMP inhibitors. Here we report that tumor-derived MMP-3 contributes to bone metastatic prostate cancer progression via intrinsic and extrinsic routes. MMP-3 ablation in prostate cancer cell lines significantly reduced in vitro growth combined with lowered AKT and ERK phosphorylation and total VEGFR1 and FGFR3 protein levels. In vivo, MMP-3 ablated tumors grew at a slower rate and were significantly less vascularized. Quantitative PCR analyses of wild type and MMP-3 silenced prostate cancer cells also demonstrate downregulation of a wide array of angiogenic factors. The extrinsic role for MMP-3 in angiogenesis was supported by in vitro endothelial tube formation assays where the lack of MMP-3 in prostate cancer conditioned media resulted in slower rates of tube formation. Taken together, our results suggest that tumor-derived MMP-3 contributes to prostate cancer growth in bone. These data indicate that selective inhibition of MMP-3 and/or targeting MMP generated products could be efficacious for the treatment of prostate to bone metastases.

Indexed as

AnimalsApoptosisBone NeoplasmsCell ProliferationDisease Models, AnimalHumansMaleMatrix Metalloproteinase 3MiceNeovascularization, PathologicProstatic NeoplasmsTumor Cells, CulturedMatrix Metalloproteinase 3MMP3 protein, humanAngiogenesisBoneMatrix metalloproteinaseMetastasisMMP-3Prostate cancer

Identifiers

PMID32896761
PMCPMC7481881
OpenAlexW3083691271

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.