Evidence map›Paper›PMID 19863778›Full record

ArticleBMC genomics2009

Anti-proliferative action of vitamin D in MCF7 is still active after siRNA-VDR knock-down.

José L Costa, Paul P Eijk, Mark A van de Wiel, Derk ten Berge, Fernando Schmitt, Carmen J Narvaez, JoEllen Welsh, Bauke Ylstra

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.3field-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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Observational
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
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  11. Article
  12. Article
  13. Cellular and molecular effects of vitamin D on carcinogenesis.Archives of biochemistry and biophysics · 2012
    Review
  14. Review
  15. Article
  16. New vitamin D analogs as potential therapeutics in melanoma.Expert review of anticancer therapy · 2012
    Review
  17. Review
  18. 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

8 authors at 4 institutions in 3 countries.

José L CostaDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands. jcosta@ipatimup.pt
Paul P Eijk
Mark A van de Wiel
Derk ten Berge
Fernando Schmitt
Carmen J Narvaez
JoEllen Welsh
Bauke Ylstra
Amsterdam UMC Location VUmc · NLUniversity at Albany, State University of New York · USErasmus MC Cancer Institute · NLUniversidade do Porto · PT

Funding

VITAMIN D MEDICATED APOPTOSIS IN MAMMARY CELLSR01CA069700 · NCI · UNIVERSITY OF NOTRE DAME · PI WELSH, JOELLEN · 1995 to 2009
$2.8M
NCI NIH HHS CA69700
6 · The paper itself

Abstract

backgroundThe active form of Vitamin D, 1,25-dihydroxyvitamin D3 (1,25D), has strong anti-proliferative effects, yet the molecular mechanisms underneath this effect remain unclear. In contrast, the molecular mechanism of 1,25D for the regulation of calcium homeostasis has principally been resolved, demonstrating a pivotal role for the vitamin D receptor (VDR).

resultsWe first addressed the question whether the anti-proliferative effects of 1,25D are influenced by VDR. Knockdown of VDR by siRNA did not affect the anti-proliferative effects of 1,25D in MCF7 breast cancer cells. This unanticipated finding led us to take an alternative approach using genome wide screens to study the molecular mechanisms of 1,25D in proliferation. For that purpose, four independently developed and stable 1,25D resistant MCF7 cell lines were analyzed. Array CGH identified a copy number alteration in a region of 13.5 Mb at chromosome 11q13.4-14.1 common to all four 1,25D resistant cell lines. Expression arrays revealed that no single gene was differentially expressed between the sensitive and resistant cells, but multiple membrane receptor signaling pathways were altered in the 1,25D resistant cell lines. Importantly, in the genome wide experiments neither VDR, CYP24A1 nor other known vitamin D signaling pathway genes were associated with 1,25D resistance.

conclusionIn conclusion, siRNA and genome wide studies both suggest that the anti-proliferative effects of 1,25D in MCF7 breast tumor cell lines do not rely on classical Vitamin D pathway per se.

Indexed as

Cell Line, TumorCell ProliferationChromosomes, Human, Pair 11Drug Resistance, NeoplasmGene DosageGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansReceptors, CalcitriolRNA, Small InterferingVitamin DReceptors, CalcitriolRNA, Small InterferingVitamin D

Identifiers

PMID19863778
PMCPMC2778664
OpenAlexW2097687592

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.