Evidence map›Paper›PMID 11313934›Full record

ArticleOncogene2001

Synergistic growth inhibition of prostate cancer cells by 1 alpha,25 Dihydroxyvitamin D(3) and its 19-nor-hexafluoride analogs in combination with either sodium butyrate or trichostatin A.

S F Rashid, J S Moore, E Walker, P M Driver, J Engel, C E Edwards, G Brown, M R Uskokovic, M J Campbell

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.3field-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

38 citing papers in PubMed, 117 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Vitamin D Receptor Signaling and Cancer.Endocrinology and metabolism clinics of North America · 2017
    Review
  10. Review
  11. Review
  12. Vitamin D receptor and RXR in the post-genomic era.Journal of cellular physiology · 2015
    Review
  13. Article
  14. Review
  15. Vitamin D and the epigenome.Frontiers in physiology · 2014
    Review
  16. Review
  17. Epigenetic distortion to VDR transcriptional regulation in prostate cancer cells.The Journal of steroid biochemistry and molecular biology · 2013
    Review
  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

9 authors at 2 institutions in 2 countries.

S F RashidDivision of Immunity & Infection, Birmingham University Medical School, Edgbaston, Birmingham, B15 2TH, UK.
J S Moore
E Walker
P M Driver
J Engel
C E Edwards
G Brown
M R Uskokovic
M J Campbell
University of Birmingham · GBLa Roche College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer is a major cause of male cancer death. In vitro and in vivo data support a role for 1 alpha,25 Dihydroxyvitamin D(3) (1 alpha,25(OH)(2)D(3)) in regulating the growth and differentiation of the normal prostate gland yet prostate cancer cells appear significantly less sensitive to this action. Vitamin D(3) receptor (VDR) content or mutational status do not correlate clearly with the antiproliferative effects of 1 alpha,25(OH)(2)D(3) and therefore it is unclear why prostate cancer cell lines are significantly less sensitive to this action. We hypothesized that the antiproliferative responses of prostate cancer cells to 1 alpha,25(OH)(2)D(3) are suppressed by a process involving histone deacetylation. Sodium butyrate (NaB) and trichostatin A (TSA) are inhibitors of histone deacetylase (HDAC) activity. Low doses of NaB or TSA (300 microM and 15 nM respectively), which alone were relatively inactive, synergized with 1 alpha,25(OH)(2)D(3) in liquid and semi-solid agar to inhibit the growth of LNCaP, PC-3 and DU-145 prostate cancer cells. Still greater synergy was observed between vitamin D(3) hexafluoride analogs and either NaB or TSA. The mechanism appeared to involve neither the cyclin-dependent kinase inhibitor, p21((waf1/cip1)) nor cell cycle arrest, but rather induction of apoptosis. These data suggest that cells dysregulate the normal pro-apoptotic signals of 1 alpha,25(OH)(2)D(3) during prostate cancer development by a mechanism involving histone deacetylation. Combination therapy with potent vitamin D(3) analogs and clinically approved HDAC inhibitors may overcome this lesion and improve the treatment of both androgen-dependent and independent prostate cancer.

Indexed as

Histone Deacetylase InhibitorsAntineoplastic AgentsApoptosisButyric AcidCalcitriolCell CycleCholecalciferolCyclin-Dependent Kinase Inhibitor p21CyclinsCytochrome P-450 Enzyme SystemDrug SynergismEnzyme InhibitorsHumansHydroxamic AcidsMaleProstatic Neoplasms19-nor-hexafluoride vitamin D3Antineoplastic AgentsButyric AcidCalcitriolCDKN1A protein, humanCholecalciferolCyclin-Dependent Kinase Inhibitor p21CyclinsCytochrome P-450 Enzyme SystemEnzyme InhibitorsHistone Deacetylase InhibitorsHydroxamic AcidsSteroid Hydroxylasestrichostatin AVitamin D3 24-Hydroxylase

Identifiers

PMID11313934
OpenAlexW2312877617

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.