Evidence map›Paper›PMID 26019137›Full record

ArticleOncotarget2015

FGF23 promotes prostate cancer progression.

Shu Feng, Jianghua Wang, Yiqun Zhang, Chad J Creighton, Michael Ittmann

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. FGF family in health and disease.Molecular biomedicine · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. The vitamin DAmerican journal of physiology. Cell physiology · 2025
    Article
  9. Article
  10. Article
  11. Emerging concepts on the FGF23 regulation and activity.Molecular and cellular biochemistry · 2025
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Metabolic Health and Disease: A Role of Osteokines?Calcified tissue international · 2023
    Review
  18. Review
  19. Article
  20. Review

3 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Shu FengDepartment of Pathology and Immunology, Baylor College of Medicine and Michael E. DeBakey Dept. of Veterans Affairs Medical Center, Houston, Texas, USA.
Jianghua WangDepartment of Pathology and Immunology, Baylor College of Medicine and Michael E. DeBakey Dept. of Veterans Affairs Medical Center, Houston, Texas, USA.
Yiqun ZhangDan L. Duncan Cancer Center Division of Biostatistics, Baylor College of Medicine, Houston, Texas, USA.
Chad J CreightonDan L. Duncan Cancer Center Division of Biostatistics, Baylor College of Medicine, Houston, Texas, USA.
Michael IttmannDepartment of Pathology and Immunology, Baylor College of Medicine and Michael E. DeBakey Dept. of Veterans Affairs Medical Center, Houston, Texas, USA.
Baylor College of Medicine · USMichael E. DeBakey VA Medical Center · US

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
NCI NIH HHS P30 CA125123
6 · The paper itself

Abstract

Prostate cancer is the most common cancer in US men and the second leading cause of cancer deaths. Fibroblast growth factor 23 (FGF23) is an endocrine FGF, normally expressed by osteocytes, which plays a critical role in phosphate homeostasis via a feedback loop involving the kidney and vitamin D. We now show that FGF23 is expressed as an autocrine growth factor in all prostate cancer cell lines tested and is present at increased levels in prostate cancer tissues. Exogenous FGF23 enhances proliferation, invasion and anchorage independent growth in vitro while FGF23 knockdown in prostate cancer cell lines decreases these phenotypes. FGF23 knockdown also decreases tumor growth in vivo. Given that classical FGFs and FGF19 are also increased in prostate cancer, we analyzed expression microarrays hybridized with RNAs from of LNCaP cells stimulated with FGF2, FGF19 or FGF23. The different FGF ligands induce overlapping as well as unique patterns of gene expression changes and thus are not redundant. We identified multiple genes whose expression is altered by FGF23 that are associated with prostate cancer initiation and progression. Thus FGF23 can potentially also act as an autocrine, paracrine and/or endocrine growth factor in prostate cancer that can promote prostate cancer progression.

Indexed as

AnimalsBlotting, WesternCell Line, TumorCell MovementCell ProliferationDisease ProgressionEnzyme-Linked Immunosorbent AssayFibroblast Growth Factor-23Fibroblast Growth FactorsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeterograftsHumansMaleMiceMice, SCIDFGF23 protein, humanFgf23 protein, mouseFibroblast Growth Factor-23Fibroblast Growth Factorsendocrine fibroblast growth factorsFGF23fibroblast growth factorsprostate cancersignal transduction

Identifiers

PMID26019137
PMCPMC4627308
OpenAlexW1527661581

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.